Biomedical subjects

D H Wasserman

Publications and source records attributed to D H Wasserman.

At least 91 records · Page 5Linked to original sources

PubMed1989

Physiological bases for the treatment of the physically active individual with diabetes.

Substrate utilisation and glucose homoeostasis during exercise is controlled by the effects of precise changes in insulin, glucagon and the catecholamines. The important role these hormones play is clearly seen in people with diabetes, as the normal endocrine response is often lost. In individuals with insulin-dependent diabetes (IDDM), there can be an increased risk of hypoglycaemia during or after exercise or, conversely, there can be a worsening of the diabetic state if insulin deficiency is present. In contrast, it appears that people with non-insulin-dependent diabetes (NIDDM) can generally exercise without fear of a deleterious metabolic response. The exercise response both in healthy subjects and in those with diabetes is dependent on many factors such as age, nutritional status and the duration and intensity of exercise. Since there are so many variables which govern individual response to exercise, an exact exercise prescription for all people with diabetes cannot be made. There are many adjustments to the therapeutic regimen which an individual with IDDM can make in order to avoid hypoglycaemia during or after exercise. In general, a reduction in insulin dosage and the added ingestion and continual availability of carbohydrates are wise precautions. On the other hand, exercise should be postponed if blood glucose is greater than 2500 mg/L and ketones are present in the urine. As more is understood about the regulation of substrate metabolism during exercise, more refined therapeutic strategies can be defined. An understanding of the metabolic response to exercise is critical for generating an effective and safe training programme for all diabetic individuals who wish to be physically active.

Diabetes Mellitus↗

PubMed1989

Exercise-induced fall in insulin and increase in fat metabolism during prolonged muscular work.

The role of the exercise-induced fall in insulin in fat metabolism was studied in dogs during 150 min of treadmill exercise alone (controls) or with insulin clamped at basal levels by an intraportal infusion to prevent the normal fall in insulin concentration (ICs). To counteract the suppressive effect of insulin on glucagon release, glucagon was supplemented by an intraportal infusion in ICs. In all dogs, catheters were placed in a carotid artery and in the portal and hepatic veins for sampling and in the vena cava and the splenic vein for infusion purposes. Glucose levels were clamped in ICs to recreate the glycemic response evident in controls. In controls, insulin fell by 7 +/- 1 microU/ml but was unchanged from basal levels in ICs (0 +/- 2 microU/ml). Glucagon, norepinephrine, epinephrine, and cortisol rose similarly in controls and ICs. Arterial free-fatty acid (FFA) levels rose by 644 +/- 126 mu eq/L in controls but did not increase in ICs (-12 +/- 148 mu eq/L). Arterial glycerol levels rose by 337 +/- 43 and 183 +/- 19 microM in controls and ICs. Hepatic FFA delivery and fractional extraction increased by 17 +/- 3 and 0.06 +/- 0.02 mumol.kg-1.min-1, respectively, in controls. In ICs, hepatic FFA delivery increased by only 1 +/- 2 mumol.kg-1.min-1, whereas hepatic fractional extraction fell slightly (-0.03 +/- 0.03). Consequently, net hepatic FFA uptake rose by 4.8 +/- 1.5 mumol.kg-1.min-1 in controls but decreased slightly in ICs (-0.5 +/- 1.1 mumol.kg-1.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Exercise-induced rise in glucagon and ketogenesis during prolonged muscular work.

These experiments examined the role of the exercise-induced increment in glucagon in the control of ketogenesis during prolonged moderate-intensity (100 m/min, 12% grade) treadmill exercise. Dogs were studied during 150 min of exercise with saline infusion alone (C; n = 6) with the glucagon levels clamped at basal values (somatostatin infusion with basal glucagon replacement and the normal fall in insulin simulated; BG; n = 5) or with the normal exercise-induced rise in glucagon simulated (somatostatin infusion with the rise in glucagon and the fall in insulin simulated; SG; n = 5). Glucose was infused as needed in SG and BG to maintain the glycemic response seen in C. In all dogs, catheters were inserted into the carotid artery and the portal and hepatic veins for blood sampling and the vena cava and the splenic vein for infusions. Glucagon rose from 62 +/- 5 and 57 +/- 4 pg/ml at rest to 104 +/- 20 and 120 +/- 12 pg/ml during exercise in C and SG but did not deviate from basal in BG (56 +/- 3 pg/ml). Insulin fell similarly from rest to the end of exercise in C (13 +/- 2 to 5 +/- 1 microU/ml), SG (11 +/- 1 to 6 +/- 1 microU/ml), and BG (10 +/- 1 to 6 +/- 1 microU/ml). In C, SG, and BG, free-fatty acid (FFA) levels rose from 941 +/- 81, 1240 +/- 155, and 938 +/- 36 mu eq/L at rest to 1615 +/- 149, 1558 +/- 175, and 1391 +/- 160 mu eq/L with exercise.2+n C,

Animals↗

PubMed1988

Importance of intrahepatic mechanisms to gluconeogenesis from alanine during exercise and recovery.

These studies were performed to assess the importance of intrahepatic mechanisms to gluconeogenesis in the dog during 150 min of treadmill exercise and 90 min of recovery. Sampling catheters were implanted in an artery and portal and hepatic veins 16 days before experimentation. Infusions of [U-14C]alanine, [3-3H]glucose, and indocyanine green were used to assess gluconeogenesis. During exercise, a decline in arterial and portal vein plasma alanine and in hepatic blood flow led to a decrease in hepatic alanine delivery. During recovery, hepatic blood flow was restored to basal, causing an increase in hepatic alanine delivery beyond exercise rates but still below resting rates. Hepatic fractional alanine extraction increased from 0.26 +/- 0.02 at rest to 0.64 +/- 0.03 during exercise and remained elevated during recovery. Net hepatic alanine uptake was 2.5 +/- 0.2 mumol.kg-1.min-1 at rest and remained unchanged during exercise but was increased during recovery. The conversion rate of [14C]alanine to glucose had increased by 248 +/- 38% by 150 min of exercise and had increased further during recovery. The efficiency with which alanine was channeled into glucose in the liver was accelerated to a rate of 338 +/- 55% above basal by 150 min of exercise but declined slightly during recovery. In conclusion, 1) gluconeogenesis from alanine is accelerated during exercise, due to an increase in the hepatic fractional extraction of the amino acid and through intrahepatic mechanisms that more efficiently channel it into glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine↗

PubMed1988

Metabolic role of the exercise-induced increment in epinephrine in the dog.

The role of the exercise-induced increment in epinephrine was studied in five adrenalectomized (ADX) and in six normal dogs (C). Experiments consisted of an 80-min equilibration period, a 40-min basal period, and a 150-min exercise period. ADX were studied with epinephrine replaced to basal levels during rest and to increased levels during exercise to simulate its normal rise (HE) and on a separate day with epinephrine maintained at basal levels throughout the study (BE). Cortisol was replaced during rest and exercise in ADX so as to simulate the levels seen in C. Glucose was infused as needed in ADX to maintain the glycemia evident during exercise in C. Glucose production (Ra) and utilization (Rd) were assessed isotopically. In C, epinephrine had risen by 95 +/- 25 pg/ml by the end of exercise. In HE, the increment in epinephrine (117 +/- 29 pg/ml) was similar to that seen in C, whereas in BE epinephrine fell by 18 +/- 9 pg/ml. Basal norepinephrine levels were 139 +/- 9, 260 +/- 25, and 313 +/- 33 pg/ml in C, HE, and BE, respectively. In response to exercise, norepinephrine increased by nearly twofold in all protocols. Basal and exercise-induced changes in plasma glucagon and insulin were similar in C and ADX. Ra increased similarly in C (5.3 +/- 0.6 mg.kg-1.min-1) and HE (4.9 +/- 0.6 mg.kg-1.min-1). In BE, Ra rose normally for the initial 90 min but then declined resulting in a rise of only 2.9 +/- 0.5 mg.kg-1.min-1 after 150 min of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗

PubMed1987

Dynamics of hepatic lactate and glucose balances during prolonged exercise and recovery in the dog.

The present experiments were undertaken to assess dynamics of hepatic lactate and glucose balance in the over-night-fasted dog during 150 min of moderate-intensity treadmill exercise and 90 min of exercise recovery. Catheters were implanted chronically in an artery and portal and hepatic veins 16 days before experimentation. 3-3H-glucose was infused to determine hepatic glucose uptake, as well as tracer-determined glucose production by isotope dilution (Ra). At rest, net hepatic lactate output was 0.33 +/- 0.15 mg.kg-1.min-1 and increased to 2.26 +/- 0.82 mg.kg-1.min-1 after 10 min of exercise, after which it fell such that the liver was a net lactate consumer by the end of exercise and through recovery. In contrast to the rapid release of lactate, net hepatic glucose output rose gradually from 2.58 +/- 0.20 mg.kg-1.min-1 at rest to 8.87 +/- 0.85 mg.kg-1.min-1 after 60 min of exercise, beyond which it did not change significantly until the cessation of exercise. Hepatic glucose uptake at rest was 1.38 +/- 0.42 mg.kg-1.min-1 and did not change appreciably during exercise or recovery. Absolute hepatic glucose output (net glucose output plus uptake) rose from 3.96 +/- 0.45 mg.kg-1.min-1 at rest to 10.20 +/- 1.09 mg.kg-1.min-1 after 60 min of exercise and was 9.65 +/- 1.15 mg.kg-1.min-1 at 150 min of exercise. Ra rose from 3.34 +/- 0.21 mg.kg-1.min-1 to 7.58 +/- 0.73 and 8.59 +/- 0.77 mg.kg-1.min-1 at 60 and 150 min, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Interaction between insulin and counterregulatory hormones in control of substrate utilization in health and diabetes during exercise.

In summary, the appropriate balance of glucagon and insulin at the liver and the catecholamines and insulin in the periphery provide the most optimal balance of substrate fluxes to the working muscle. When the hormonal balance is perturbed such as is seen in diabetes or with glucagon suppression, or when the effect of a hormone is impaired such as with beta blockade, optimal substrate balance is lost. The effects of these hormones can be overridden by metabolic factors in muscle, as evidenced by the uncoupling of the normal catecholamine antagonism of glucose uptake from the actual glucose uptake observed during exercise under conditions of tissue hypoxia.

Animals↗

PubMed1986

Glucose turnover in response to exercise during high- and low-FIO2 breathing in man.

The purpose of this study was to assess whether breathing high or low concentrations of O2 could affect glucose turnover during exercise in man. Ten healthy subjects performed two constant work-rate exercise tests, one when the fraction of inspired O2 (FIO2) was 0.15 and the other at the same work rate but when the FIO2 was 0.80. The work rate for each subject was chosen so that blood lactate would be elevated during hypoxia, but would be lower during hyperoxia. Glucose appearance (Ra) and disappearance (Rd) were measured using the primed, constant infusion of [3-3H]glucose. Although the work rate was the same during hypoxia and hyperoxia in each subject, hypoxic exercise was accompanied by a significantly larger rest to exercise increase in Rd (delta Rd) compared with hyperoxia by 265%. Similarly, delta Ra was greater during hypoxia than during hyperoxia by 188%. Lactate to pyruvate ratios were significantly higher during hypoxic exercise suggesting a shift in the cell redox to a more reduced state. Insulin and glucagon were not affected by the FIO2, but both epinephrine and norepinephrine were increased during hypoxic exercise, which may explain the increase in Ra. The regulation of blood glucose during exercise in vivo appears to be dependent on the availability of oxygen to the working muscle cells.

Adult↗

PubMed1986

Calculation of metabolic fluxes with anatomically separated sources of tracer and tracee.

Traditional calculations of metabolic fluxes using isotope dilution are based on the assumption that tracer and tracee enter the distribution space through effectively identical ports. If the tracer infusion site is not identical with the site of endogenous release of the tracee, the traditional equations for calculating rate of appearance (Ra) of a metabolite may give rise to appreciable errors due to the presence of gradients in specific activity. When tracer and tracee enter by means of anatomically disparate sites, such as may be encountered in the study of metabolite (e.g., lactate, alanine, and glycerol) or free fatty acid turnover, one must employ a modification of the traditional specific activity. This modified specific activity is obtained as the ratio of tracer concentration "near" (in the same compartment as) the source of tracee to the concentration of tracee near the source of tracer infusion. This concept is employed to derive equations for calculating metabolic turnover in both steady- and non-steady-state conditions when entry sites of tracer and tracee are dissimilar.

Glucose↗

PubMed1985

Effect of hematocrit reduction on hormonal and metabolic responses to exercise.

We wished to determine the effect of a 25% hematocrit reduction on glucoregulatory hormone release and glucose fluxes during exercise. In five anemic dogs, plasma glucose fell by 21 mg/dl and in five controls by 7 mg/dl by the end of the 90-min exercise period. After 50 min of exercise, hepatic glucose production (Ra) and glucose metabolic clearance rate (MCR) began to rise disproportionately in anemics compared with controls. By the end of exercise, the increase in Ra was almost threefold higher (delta 15.1 +/- 3.4 vs. delta 5.2 +/- 1.3 mg X kg-1 X min-1) and MCR nearly fourfold (delta 24.6 +/- 8.8 vs. delta 6.5 +/- 1.3 ml X kg-1 X min-1). Exercise with anemia, in relation to controls resulted in elevated levels of glucagon [immunoreactive glucagon (IRG) delta 1,283 +/- 507 vs delta 514 +/- 99 pg/ml], norepinephrine (delta 1,592 +/- 280 vs. delta 590 +/- 155 pg/ml), epinephrine (delta 2,293 +/- 994 vs. delta 385 +/- 186 pg/ml), cortisol (delta 6.7 +/- 2.2 vs. delta 2.1 +/- 1.0 micrograms/dl) and lactate (delta 12.1 +/- 2.2 vs. delta 4.2 +/- 1.8 mg/dl) after 90 min. Immunoreactive insulin and free fatty acids were similar in both groups. In conclusion, exercise with a 25% hematocrit reduction results in 1) elevated lactate, norepinephrine, epinephrine, cortisol, and IRG levels, 2) an increased Ra which is likely related to the increased counterregulatory response, and 3) we speculate that a near fourfold increase in MCR is related to metabolic changes due to hypoxia in working muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Anemia↗

PubMed1985

Important role of glucagon during exercise in diabetic dogs.

To define the role of immunoreactive glucagon (IRG) during exercise in diabetes, 12 insulin-deprived alloxan-diabetic (A-D) dogs were run for 90 min (100 m/min, 12 degrees) with or without somatostatin (St 0.5 microgram . kg-1 . min-1). Compared with normal dogs, A-D dogs were characterized by similar hepatic glucose production (Ra), lower glucose metabolic clearance, and higher plasma glucose and free fatty acid levels during rest and exercise. In A-D dogs IRG was greater at rest and exhibited a threefold greater exercise increment than controls, whereas immunoreactive insulin (IRI) was reduced by 68% at rest but had similar values to controls during exercise. Basal norepinephrine, epinephrine, cortisol, and lactate levels were similar in normal and A-D dogs. However, exercise increments in norepinephrine, cortisol, and lactate were higher in A-D dogs. When St was infused during exercise in the A-D dogs, IRG was suppressed by 432 +/- 146 pg/ml below basal and far below the exercise response in A-D controls (delta = 645 +/- 153 pg/ml). IRI was reduced by 1.8 +/- 0.2 microU/ml with St. With IRG suppression the increase in Ra seen in exercising A-D controls (delta = 4.8 +/- 1.6 mg . kg-1 . min-1) was virtually abolished, and glycemia fell by 104 to 133 +/- 37 mg/dl. Owing to this decrease in glycemia, the increase in glucose disappearance was attenuated. Despite the large fall in glucose during IRG suppression, counterregulatory increases were not excessive compared with A-D controls. In fact, as glucose levels approached euglycemia, the increments in norepinephrine and cortisol were reduced to levels similar to those seen in normal exercising dogs. In conclusion, IRG suppression during exercise in A-D dogs almost completely obviated the increase in Ra, resulting in a large decrease in plasma glucose. Despite this large fall in glucose, there was no excess counterregulation, since glucose concentrations never reached the hypoglycemic range.

Animals↗

PubMed1985

Role of beta-adrenergic mechanisms during exercise in poorly controlled diabetes.

To examine the beta-adrenergic effects of the catecholamines in poorly controlled diabetes, we have studied insulin-deprived alloxan-diabetic (A-D) dogs during 90 min of moderate exercise (100 m/min, 10-12 degrees) alone (C) or with propranolol (5 micrograms . kg-1 . min-1) (P) or combined P and somatostatin infusion (0.5 microgram . kg-1 . min-1) (P + St). In P, in contrast to C, immunoreactive glucagon (IRG) rose only after 50 min of exercise. However, hepatic glucose production (Ra) rose normally. In P + St, IRG fell 50% below basal, and the Ra response to exercise was abolished. Interestingly, in P and P + St, glucose metabolic clearance rate (MCR) rose by 400% above the inadequate MCR response to exercise in C, despite 30% lower insulin levels. Compared with C, free fatty acids (FFA) and lactate were sharply reduced during P and P + St. Plasma glucose (G) did not change in C, but due to elevated glucose uptake, G fell over 120 mg/dl in P, and due to diminished Ra, G fell 170 mg/dl in P + St. Norepinephrine was similar in all groups. Epinephrine and cortisol were higher in P + St by 90 min of exercise, perhaps as a result of hypoglycemia. In summary, during exercise in poorly controlled A-D dogs, beta-blockade does not appear to affect Ra; beta-blockade leads to diminished mobilization of extrahepatic substrate as evidenced by reduced FFA and lactate levels; beta-blockade increases MCR to levels seen in normal dogs during exercise alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Interactions between glucagon and other counterregulatory hormones during normoglycemic and hypoglycemic exercise in dogs.

Somatostatin (ST)-induced glucagon suppression results in hypoglycemia during rest and exercise. To further delineate the role of glucagon and interactions between glucagon and the catecholamines during exercise, we compensated for the counterregulatory responses to hypoglycemia with glucose replacement. Five dogs were run (100 m/min, 12 degrees) during exercise alone, exercise plus ST infusion (0.5 micrograms/kg-min), or exercise plus. ST plus glucose replacement (3.5 mg/kg-min) to maintain euglycemia. During exercise alone there was a maximum increase in immunoreactive glucagon (IRG), epinephrine (E), norepinephrine (NE), FFA, and lactate (L) of 306 +/- 147 pg/ml, 360 +/- 80 pg/ml, 443 +/- 140 pg/ml, 541 +/- 173 mu eq/liter, and 6.3 +/- 0.7 mg/dl, respectively. Immunoreactive insulin (IRI) decreased by 10.2 +/- 4 micro/ml and cortisol (C) increased only slightly (2.1 +/- 0.3 micrograms/dl). The rates of glucose production (Ra) and glucose uptake (Rd) rose markedly by 6.6 +/- 2.2 mg/kg-min and 6.2 +/- 1.5 mg/kg-min. In contrast, when ST was given during exercise, IRG fell transiently by 130 +/- 20 pg/ml, Ra rose by only 3.6 +/- 0.5 mg/kg-min, and plasma glucose decreased by 29 +/- 6 mg/dl. The decrease in IRI was no different than with exercise alone (10.2 +/- 2.0 microU/ml). As plasma glucose fell, C, FFA, and L rose excessively to peaks of 5.4 +/- 1.3 micrograms/dl, 1,166 +/- 182 mu eq/liter and 15.5 +/- 7.0 mg/dl. The peak increment in E (765 +/- 287 pg/ml) coincided with the nadir in plasma glucose and was four times greater than during normoglycemic exercise. Hypoglycemia did not affect the rise in NE. The increase in Rd was attenuated and reached a peak of only 3.7 +/- 0.8 mg/kg-min. During glucose replacement, IRG decreased by 109 +/- 30 pg/ml and the IRI response did not differ from the response to normal exercise. Ra rose minimally by 1.5 +/- 0.3 mg/kg-min. The changes in E, C, Rd, and L were restored to normal, whereas the FFA response remained excessive. In all protocols increments in Ra were directly correlated to the IRG/IRI molar ratio while no correlation could be demonstrated between epinephrine or norepinephrine and Ra. In conclusion, (a) glucagon controlled approximately 70% of the increase of Ra during exercise. This became evident when counterregulatory responses to hypoglycemia (E and C) were obviated by glucose replacement; (b) increments in Ra were strongly correlated to the IRG/IRI molar ratio but not the plasma catecholamine concentration; (c) the main role of E in hypoglycemia was to limit glucose uptake by the muscle; (d) with glucagon suppression, glucose production was deficient but a further decline of glucose was prevented through the peripheral effects of E, (e) the hypoglycemic stimulus for E secretion was facilitated by exercise; and (f) we hypothesize that an important role of glucagons during exercise could be to spare muscle glycogen by stimulating glucose production by the liver.

Animals↗

PubMed1984

Vascular injuries.

Decisive management of peripheral vascular trauma will maximize patient survival and limb salvage. Diagnosis rests upon an acute clinical awareness, supplemented by the appropriate use of noninvasive techniques and contrast radiography. Priorities must be established in the management of associated injuries, and delay must be avoided when ischemic changes are present. Early surgical consultation is essential.

Adolescent↗

PubMed1983

Ultrasonic imaging and oculoplethysmography in diagnosis of carotid occlusive disease.

Pulsed Doppler ultrasonic imaging (UI) of the cervical carotid artery provides flow-dependent anatomic detail of the carotid bifurcation, while oculoplethysmography (Kartchner) (OPG-K) and ocular pneumoplethysmography (Gee) (OPG-G) reflect changes in flow and pressure resulting from hemodynamically significant lesions. We examined 66 patients prospectively with UI, OPG-K, and OPG-G to compare the relative accuracy of these techniques with contrast arteriography. Both UI and OPG-G were significantly more accurate than OPG-K. While the accuracies of UI and OPG-G were not significantly different, their combined use resulted in a significant increase in sensitivity compared with that of Doppler imaging alone. In addition, UI correctly identified 22 (85%) of 26 occlusions of the internal carotid artery. The use of UI and OPG-G together provided accurate anatomic and hemodynamic information useful in the evaluation of carotid occlusive disease.

Arterial Occlusive Diseases↗

PubMed1983

Coupling of ventilation to pulmonary gas exchange during nonsteady-state work in men.

During steady-state exercise, ventilation increases in proportion to CO2 output (VCO2), regulating arterial PCO2. To characterize the dynamics of ventilatory coupling to VCO2 and O2 uptake (VO2) in the nonsteady-state phase, seven normal subjects performed constant-load cycle ergometry to a series of subanaerobic threshold work rates. Each bout consisted of eight 6-min periods of alternating loaded and unloaded cycling. Ventilation and gas exchange variables were computed breath by breath, with the time-averaged response dynamics being established off-line. Ventilation increased as a linear function of VCO2 in all cases, the relationship being identical in the steady- and the nonsteady-state phases. Ventilation, however, bore a curvilinear relation to VO2, the kinetics of the latter being more rapid. Owing to the kinetic disparity between expired minute ventilation (VE) and VO2, there was an overshoot in the direction of change in VE/VO2 and end-tidal PO2 during the work-rate transition. In contrast, there was no overshoot in the direction of change in VE/VCO2 and end-tidal PCO2 throughout the nonsteady-state period. These data suggest that the exercise hyperpnea is coupled to metabolism in men via a signal proportional to VCO2 in both the nonsteady and steady states of moderate exercise.

Adolescent↗

PubMed1982

Superiority of the femoral artery of monitoring. A prospective study.

Continuous hemodynamic monitoring and ease of blood sampling are advantages of indwelling arterial catheters. The use and associated morbidity of arterial monitoring catheters were studied prospectively. Ninety-five percent of patients catheterized had multiple injuries, and almost 75 percent were 40 years of age or younger. Major and minor complication rates were similar with radial and femoral catheters, while the longevity of femoral catheters was almost twice that of radial catheters. Radial catheter-related sepsis did not occur when the duration of catheterization was less than 4 days. Tissue loss secondary to radical catheters can be minimized by immediate catheters can be minimized by immediate catheter removal upon appearance of ischemic changes. Our data support the preferential use of the femoral artery for long-term monitoring catheters in a younger patient population.

Arm↗

PubMed1976

Seminoma in male aged seventy-three.

This is a report of a seventy-three-year-old male found to have a seminomatous tumor of his left testicle. This may represent the oldest reported case of pure seminoma. Men of all ages should have careful palpation of the testicles as part of a physical examination.

Aged↗