The effects of a commercial dietary supplement on human performance.

Twenty male runners were recruited to test whether a commercial ergogenic supplement was of any physiological benefit to endurance performance. Either a placebo or the supplement (a vitamin, mineral, amino acid, and unsaturated fatty acid complex) was administered to the subjects in a dose of three capsules daily over a 4-wk period in a double-blind design. A 60-min submaximal treadmill run (65 to 70% VO2 max) and a max VO2 test were completed by each subject before and after supplementation. The results demonstrated that even though exercise caused a significant decrease in muscle glycogen (36 to 48%) and blood glucose (24 to 34%) levels and an increase in blood free fatty acid (350%) and lactate concentration (200 to 230%), these changes were similar for both placebo and supplement groups. Similarly, the supplement had no effect on maximum oxygen consumption. We conclude that the supplement had no beneficial effect on performance as indicated by its inability to alter significantly any of the metabolic or physiological parameters, and that supplements of this nature are of no physiological value to the athlete who consumes a normal nutritionally balanced diet.

Effects of cocaine, exercise, and resting conditions on plasma corticosterone and catecholamine concentrations in the rat.

Cocaine and exercise are both known as stressors, but little is known about the combined effects of these two treatments. In this study, rats under the influence of cocaine (12.5 mg/kg, intraperitoneally [IP]) or saline were exposed to a variety of resting conditions, as well as exercise (running, 26 m/min, 10% grade, for 30 minutes), to evaluate the amount of stress imposed by these conditions as determined by the changes in the plasma concentrations of corticosterone (C) and catecholamines (norepinephrine [NE], epinephrine [E], dopamine [DA]). After injection of saline, resting near the operating treadmill for 30 minutes caused the concentration of C to increase from 0.07 +/- 0.03 to 0.30 +/- 0.05 microgram/mL (P less than .05), compared to the increase to only 0.15 +/- 0.04 micrograms/mL after resting in a cage. This increase due to proximity to the treadmill subsided after 50 minutes. After cocaine, the 30-minute resting values were 0.70 +/- 0.15 (treadmill) and 0.55 +/- 0.13 (cage) (P less than .05), and did not subside after 50 minutes. Cocaine also increased levels of E, NE, and DA above those in saline under all rest conditions. With exercise, the value for C in saline increased to 0.61 +/- 0.18, but, in cocaine, the value went to 0.93 +/- 0.05 (P less than .05). The concentrations of E (946 +/- 74 v 603 +/- 101 pg/mL, cocaine v saline) and NE (1,027 +/- 102 v 440 +/- 153, cocaine v saline) during exercise also were exaggerated by cocaine treatment (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Cocaine does not alter cardiac glycogen content at rest or during exercise.

Cocaine is a potent sympathomimetic drug, and has been implicated as a causative factor in cardiac seizures. However, little is known about the effect of the drug on myocardial substrate utilization. In the present study, rats were injected intravenously with saline solution or one of three doses of cocaine-HCl (1.25, 5.0, 10.0 mg/kg) and subsequently rested or exercised (22 m/min at 15% grade) for 20 minutes. Hearts were removed and frozen within 30 seconds after the injection of anesthetic and within 10 seconds after opening the thoracic cavity. The mean values for resting glycogen content ranged from 24.9 to 27.0 mumol/g, and for glucose-6-phosphate, from 0.27 to 0.30 mumol/g across groups. These values were unaffected by cocaine or exercise. We conclude, based on the conditions of this study, that cocaine has no direct or indirect effect on glycogen storage of the myocardium at rest or during exercise.

Glycogen repletion and exercise endurance in rats adapted to a high fat diet.

It is well accepted that exercise endurance is directly related to the amount of carbohydrate stored in muscle and that a low carbohydrate diet reduces glycogen storage and exercise performance. However, more recent evidence has shown that when the organism adapts to a high fat diet endurance is not hindered. The present study was designed to test that claim and to further determine if animals adapted to a high fat diet could recover from exhausting exercise and exercise again in spite of carbohydrate deprivation. Fat-adapted (3 to 4 weeks, 78% fat, 1% carbohydrates) rats (FAT) ran (28 m/min, 10% grade) as long as carbohydrate-fed (69% carbohydrates) animals (CHO) (115 v 109 minutes, respectively) in spite of lower pre-exercise glycogen levels in red vastus muscle (36 v 54 mumols/g) and liver (164 v 313 mumols/g) in the FAT group. Following 72 hours of recovery on the FAT diet, glycogen in muscle had replenished to 42 mumols/g (v 52 for CHO) and liver glycogen to 238 mumols/g (v 335 for CHO). The animals were run to exhaustion a second time and run times were again similar (122 v 132 minutes FAT v CHO). When diets were switched after run 1, FAT-adapted animals, which received carbohydrates for 72 hours, restored muscle and liver glycogen (48 and 343 mumols/g, respectively) and then ran longer (144 minutes) than CHO-adapted animals (104 minutes) that ate fat for 72 hours and that had reduced glycogen repletion. We conclude that, in contrast to the classic CHO loading studies in humans that involved acute (72 hours) fat feedings and subsequently reduced endurance, rats adapted to a high fat diet do not have a decrease in endurance capacity even after recovery from previous exhausting work bouts. Part of this adaptation may involve the increased storage and utilization of intramuscular triglycerides (TG) as observed in the present experiment.

Effect of cocaine on exercise endurance and glycogen use in rats.

To determine the effects of cocaine on exercise endurance, male rats were injected intraperitoneally with cocaine (20 mg/kg body wt) or saline and then run to exhaustion 20 min later at 22 m/min and 15% grade. Saline-injected animals ran 74.9 +/- 16.5 (SD) min, whereas cocaine-treated rats ran only 29 +/- 11.6 min. The drug had no effect on resting blood glucose or lactate levels, nor did it affect resting glycogen levels in liver or red and white vastus muscle. However, it did reduce resting soleus glycogen content by 30%. During exercise liver and soleus glycogen depletion occurred at the same rate in saline- and cocaine-treated animals. In contrast, the rate of glycogen depletion during exercise in red and white vastus was markedly increased in cocaine-treated rats with a corresponding elevation in blood lactate (12 vs. only 5 mM in saline group) at exhaustion. These data suggest that cocaine administration (20 mg/kg) before submaximal exercise dramatically alters glycogen metabolism during exercise, and this effect has a negative impact on exercise endurance.

Effects of cocaine on plasma catecholamine and muscle glycogen concentrations during exercise in the rat.

This study was designed to test the hypothesis that cocaine (C) alters the normal physiological responses to exercise. Male rats were injected with saline (S) or C (12.5 mg/kg) either intravenously (iv) or intraperitoneally (ip). After injection the animals were allowed to rest for 30 min or were run on the treadmill (26 m/min, 10% grade). At rest plasma epinephrine values were 245 +/- 24 pg/ml in the S group and 411 +/- 43 (ip) and 612 +/- 41 (iv) pg/ml in the C groups (P less than 0.05 between S and C). During exercise plasma epinephrine levels were 615 +/- 32 pg/ml in S and 1,316 +/- 58 (ip) and 1,208 +/- 37 (iv) pg/ml in the C groups (P less than 0.05 between S and C). Similar results were obtained for norepinephrine. Glycogen content in the white vastus lateralis muscle was reduced to 31 +/- 2 mumol/g in S after exercise, but after C and exercise the values were 12 +/- 4 (ip) and 16 +/- 3 (iv) mumol/g (P less than 0.05 between S and C). There was no effect of the drug on this parameter at rest. Blood lactate rose to 4.8 +/- 1.0 (ip) and 5.8 +/- 1.3 (iv) mM in the C groups but to only 3.0 +/- 0.2 in the S group after exercise (P less than 0.05 between S and C). These results show that C and exercise combined exert a more dramatic effect on plasma catecholamine, muscle glycogen, and blood lactate concentrations than do C and exercise alone. They provide further insight into explaining the adverse effects of C on exercise endurance observed previously (Bracken et al., J. Appl. Physiol. 66: 377-383, 1989).

Effect of maternal exercise on fetal liver glycogen late in gestation in the rat.

To determine the effect of maternal exercise on fetal liver glycogen content, fed and fasted rats that were pregnant for 20.5 or 21.5 days were run on a rodent treadmill for 60 min at 12 m/min with a 0% grade or 16 m/min up a 10% grade. The rats were anesthetized by intravenous injection of pentobarbital sodium, and fetal and maternal liver and plasma samples were collected and frozen. Fetal liver glycogenolysis did not occur as a result of maternal exercise. Fetal blood levels of lactate increased 22-60%, but glucose, plasma glucagon, and insulin were unchanged during maternal exercise. Maternal liver glycogen decreased as a result of exercise in all groups of rats except the fasted 20.5-day-pregnant group. Plasma free fatty acids increased in all groups and blood lactate increased in fed (20.5 days) and fasted (21.5 days) pregnant rats. Maternal glucose, glucagon, and insulin values remained constant during exercise. The fetus appears to be well-protected from metabolic stress during moderate-intensity maternal exercise.

Cocaine alters myosin isoform expression in the rat soleus.

The purpose of this study was to determine whether chronic cocaine administration alters the expression of myosin isoforms in the rat soleus. Forty-five adult Sprague-Dawley rats were divided into three groups: chronic cocaine (n = 15), 12.5 mg/kg cocaine-HCl injected intraperitoneally twice daily for 14 days and one injection of cocaine (12.5 mg/kg ip) on day 15; acute cocaine (n = 15), saline injections twice daily for 14 days and one injection of cocaine (12.5 mg/kg ip) on day 15; and chronic saline (n = 15), saline injections twice daily for 14 days and one saline injection on day 15. Myosin isoform content of the soleus (native and heavy chains) was identified by electrophoresis. The solei samples from the chronic saline and acute cocaine animals contained slow myosin only. However, solei samples from the chronic cocaine group contained slow myosin and two to three other myosin isoforms and the associated heavy chains IIa and IIx. Therefore, chronic cocaine administration causes in the rat soleus a shift in myosin expression from slow isoforms to fast isoforms.

Cocaine and exercise: alteration in carbohydrate metabolism in adrenodemedullated rats.

The combined treatment of cocaine-exercise (CE) causes an exaggerated catecholamine response, a rapid depletion of muscle glycogen, and accumulation of lactic acid. To assess the contribution of the adrenal medulla in the catecholamine response and to determine the role of epinephrine (Epi) on carbohydrate metabolism, cocaine (20 mg/kg ip) or saline was injected into sham-operated (Sham) or adrenodemedullated (AdM) rats, which then ran for 5 min at 56 m/min, 0% grade. In Sham rats, CE caused plasma Epi values (means +/- SE) to rise to 27.7 +/- 6.9 nM compared with 13.3 +/- 1.5 nM in saline-exercise (SE) and 0.8 +/- 0.2 nM in both AdM-CE and AdM-SE animals (P < 0.05). With minimal Epi in AdM, CE still caused glycogen to fall to lower levels (25.4 +/- 3.0 mumol/g vs. 40.5 +/- 2.4 mumol/g) and lactate to rise to higher levels (17 +/- 3 vs. 9 +/- 1 mumol/kg) in white vastus muscle than in SE group (P < 0.05). CE had no significant effect on soleus and red vastus glycogenolysis but it did cause lactate accumulation in red vastus. As a result, plasma lactate levels were also higher after CE compared with SE in AdM (17.9 +/- 2.0 vs. 8.5 +/- 0.5 mM, P < 0.05). We conclude that during CE 1) Epi is not essential to the alteration in carbohydrate metabolism; 2) the latter may be related to the other catecholamines; 3) the adrenal medulla is the only source of Epi; and 4) the adrenal medulla is not the source of the increased levels of norepinephrine or dopamine.

Cocaine and exercise: alpha-1 receptor blockade does not alter muscle glycogenolysis or blood lactacidosis.

In our previous work, we routinely observed that a combined cocaine-exercise challenge results in an abnormally rapid muscle glycogen depletion and excessive blood lactacidosis. These phenomena occur simultaneously with a rapid rise in norepinephrine and in the absence of any rise in epinephrine. We postulated that norepinephrine may cause vasoconstriction of the muscle vasculature through activation of alpha-1 receptors during cocaine-exercise, thus inducing hypoxia and a concomitant rise in glycogenolysis and lactate accumulation. To test this hypothesis, rats were pretreated with the selective alpha-1-receptor antagonist prazosin (P) (0.1 mg/kg iv) or saline (S). Ten minutes later, the animals were treated with cocaine (-C) (5 mg/kg iv) or saline (-S) and run for 4 or 15 min at 22 m/min at 10% grade. In the S-S group, glycogen content of the white vastus lateralis muscle was unaffected by exercise at both time intervals, whereas in S-C rats glycogen was reduced by 47%. This effect of cocaine-exercise challenge was not attenuated by P. Similarly, blood lactate concentration in S-C rats was threefold higher than that of S-S after exercise, a response also not altered by pretreatment with P. On the basis of these observations, we conclude that the excessive glycogenolysis and lactacidosis observed during cocaine-exercise challenge is not the result of vasoconstriction secondary to norepinephrine activation of alpha-1 receptors.

Effect of various doses of cocaine on endurance capacity in rats.

To determine the effects of a variety of doses of cocaine on endurance capacity, rats were injected intraperitoneally with either 0.1, 0.5, 2.5, 12.5, or 20 mg/kg body wt 20 min before running to exhaustion at 26 m/min up a 10% grade. Animals given saline ran 116 +/- 9 (SE) min. At doses of 12.5 and 20 mg/kg, cocaine reduced endurance time significantly (34 and 74%, respectively). At rest the drug had no effect on liver or fast-twitch muscle glycogen but significantly reduced (20-40%) soleus glycogen at the two highest doses. However, at exhaustion, the quantity of glycogen depleted in the fast-twitch red and white vastus muscles was similar in all groups despite the reduced run times of the animals receiving a higher dose implying a greater rate of glycogenolysis due to cocaine. Blood lactate in the 20 mg/kg group (9.9 +/- 1.2 mM) at exhaustion was nearly twice that of the saline controls at exhaustion (5.1 +/- 0.6). Before exercise plasma norepinephrine (at doses of 2.5, 12.5 and 20 mg/kg) was higher than saline controls and remained higher (20 mg/kg groups) at exhaustion. We conclude that high doses of cocaine cause rapid muscle glycogen depletion and early fatigue. The mechanism by which cocaine causes these effects is not clear.

Effects of exercise on insulin-induced hypoglycemia.

The purpose of this study was to determine the effect of exercise on the rate of onset of hypoglycemia induced by infusion of excess insulin (0.8 mU.min-1.100 g-1). Rats were either fasted overnight (FS) or fed ad libitum (FD). FS rats were killed after 5, 10, or 15 min of infusion at rest or after running on the treadmill at 21 m/min and 15% grade. FD rats were killed after 10, 20, or 40 min of infusion at rest or after exercise. Rats were also killed 15 min postexercise for FS and 60 or 120 min postexercise for FD with continued insulin infusion. The progressive decline in blood glucose was not altered by exercise in the FS rats. FD rats showed a significant difference due to exercise only after 40 min (rest 4.2 +/- 0.3 mM, exercise 3.2 +/- 0.2 mM). A significant postexercise repletion of glycogen was observed in red vastus and soleus muscles of FD rats despite the decreasing blood glucose values. These data indicate that exercise accelerates the rate of development of hypoglycemia in FD rats. In the FS rats, where the rate of decline in blood glucose was greater, exercise had no effect on the time course of development of hypoglycemia.

Effects of 24-hour fast on cycling endurance time at two different intensities.

Ten competitive cyclists were exercised to exhaustion to test the potential of a 24-h fast for increasing endurance. One group (n = 4) was tested at an initial intensity of 86% maximum O2 uptake (VO2max) (HI) and a second group (n = 6) at 79% VO2max (MI). Both groups repeated test rides in fasted and normal-diet conditions. Time to fatigue was designated at two points: fatigue 1 occurred when pedal frequency could not be maintained at the initial percent VO2max; fatigue 2 occurred when pedal frequency could not be maintained at a workload of approximately 65% VO2max. In both HI and MI the 24-h fast had no effect on resting muscle glycogen stores but significantly increased plasma free fatty acid (FFA) levels. Despite the increased FFA availability, time to fatigue was reduced in the fasted groups. Fatigue 1 and 2 times (mean +/- SE) for HI-fasted were 42.0 +/- 6.2 and 170.0 +/- 20.4 min, respectively, compared with those of the HI-normal diet of 115.3 +/- 25.6 and 201.0 +/- 14.8 min. Fatigue 1 and 2 times for MI-fasted were 142.0 +/- 19.6 and 167.5 +/- 10.5 min compared with those of the MI-normal diet of 191.3 +/- 25.0 and 214.3 +/- 18.9 min. The cause of fatigue at fatigue 1 was not readily apparent. Fatigue 2 in all groups seemed to be related to hypoglycemia as well as muscle glycogen depletion.

Effects of phosphate loading on leg power and high intensity treadmill exercise.

Stim-O-Stam is a commercial ergogenic aid purported to improve human performance by reducing recovery time and enhancing endurance. The tablets contain a mixture of sodium acid phosphate and potassium phosphate. In this study, under a double-blind cross-over design, 11 male subjects underwent acute (1.24 g one hour before exercise) and chronic (3.73 g X d-1 for 6 d prior to exercise) consumption of Stim-O-Stam to determine the effects of phosphate loading on: treadmill endurance time; treadmill endurance time after 15 min of recovery from first treadmill run; leg power measured for 1 min on the Cybex device; leg power after 10 min recovery from first power test; and oxygen uptake during the treadmill run. Run times ranged from 172 to 183 s on run 1 and 145 to 152 s for run 2. Leg power averaged 62 W for both tests. Oxygen uptake averaged 52 ml X kg-1 X min-1 under all conditions. Analysis of variance showed that there was no significant effect of acute or chronic ingestion of phosphate tablets beyond that of the placebo treatment on any of the performance tests. These results argue against the claim of ergogenic benefits ascribed to this nutritional supplement.

Effects of cocaine on glycogen metabolism and endurance during high intensity exercise.

Because cocaine causes a rapid sympathetic response and central euphoria, we tested whether it would improve endurance or alter carbohydrate metabolism during high-intensity activity. Thirty male rats (10 animals/group) were injected intraperitoneally with either saline (S) or one of two doses of cocaine-HCl (12.5 (C-1) or 20.0 (C-2) mg.kg-1 b.w.). Ten minutes later they began gradually running on a rodent treadmill. Within 2 min they were running at 56 m.min-1 until fatigued. The run time to exhaustion (mean +/- SE) for C-2 (569 +/- 97 s) was less than S (859 +/- 71) and C-1 (923 +/- 65) (P < 0.05) and 25% shorter (marginally insignificant) than a pretreatment run (754 +/- 67 s) (P > 0.05). Plasma lactate concentrations at exhaustion were 4.0 +/- 0.5 (S), 7.3 +/- 1.1 (C-1), and 13.9 +/- 2.5 (C-2) mmol (P < 0.05, S vs C-2). Lactate concentrations in white vastus muscle were also elevated by C (4.7 +/- 0.6 (S), 8.1 +/- 1.3 (C-1), and 15.0 +/- 3.7 (C-2) mumol.g-1, (P < 0.05, S vs C-2)], which correlated with the reduction in glycogen content in both C groups (9.9 +/- 2.3 (C-2), 10.3 +/- 1.2 (C-1), vs 33.9 +/- 2.0 (S) mumol.g-1]. These results show that, in spite of its purported stimulatory effect, cocaine treatment (20 mg.kg-1) immediately prior to intense exercise causes accelerated glycogen degradation and lactate accumulation in white vastus muscle during exercise and premature fatigue.

Stroke volume does not plateau during graded exercise in elite male distance runners.

UNLABELLED: Stroke volume (SV) responses during graded treadmill exercise were studied in 1) elite male distance runners (N = 5), 2) male university distance runners (N = 10), and 3) male untrained university students (N = 10). METHODS: Cardiac output (Q) and SV were determined by a modified acetylene rebreathing procedure. RESULTS: There were no differences in SV responses among the three groups during the transition from rest to light exercise (P > 0.05). However, the rates of change of SV during light to maximal exercise in untrained subjects (slope = -0.1544 mL x beat(-1)) and university distance runners (slope = 0.1041) did not change, whereas it dramatically increased (P < 0.001) in elite distant runners (slope = 0.6734). Moreover, the elite distance runners showed a further slope increase in SV when heart rate was above 160 bpm, which resulted in an average maximal SV of 187 +/- 14 mL x beat(-1) compared with 145 +/- 8 and 128 +/- 14 mL x beat(-1) in the university runners and untrained students, respectively (P < 0.001). Similarly, max Q reached 33.8 +/- 2.3, 26.3 +/- 1.7, and 21.3 +/- 1.5 L x min(-1) in the three groups, respectively (P < 0.001). On the other hand, there was a nonsignificant tendency for maximal arteriovenous oxygen content difference to be lower in the elite athletes compared with the other groups. CONCLUSION: Results from university distance runners and untrained university students support the classic observation that SV plateaus at about 40% of maximal oxygen consumption despite increasing intensity of exercise. In contrast, stroke volume in the elite athletes does not plateau but increases continuously with increasing intensity of exercise over the full range of the incremental exercise test.

Cocaine and exercise: physiological responses of cocaine-conditioned rats.

To compare the physiological response to a cocaine-exercise challenge in cocaine-conditioned animals with that of acute-cocaine animals, rats were injected i.p. with either cocaine (20 mg.kg-1) or saline, twice daily for 14 consecutive days. On the 15th day (test day) cocaine-conditioned rats received an i.v. injection of cocaine (5 mg.kg-1) (chronic group). One-half of the chronic saline rats also received the cocaine injection (acute group), while the other half received saline (saline group). Immediately after injection, all rats were either rested or exercised (22 m.min-1, 10% grade) for 30 min. For most parameters there was no difference between the responses of the chronic and acute cocaine groups at rest or to the cocaine-exercise challenge. During exercise, both cocaine groups had similarly higher lactate values than the saline animals (P < 0.05). Both groups had similarly greater reductions in glycogen content of the white and red vastus muscles than occurred in the saline group; and both groups had similar increases in corticosterone. In contrast, cocaine-conditioned animals had a greater rise in norepinephrine (P < 0.059) and epinephrine (P < 0.001) in response to cocaine-exercise than did the acute group. The mechanism responsible for the exaggerated catecholamine response in the chronic cocaine animals is unknown.

Consequences of combining strength and endurance training regimens.

A common belief among many clinicians and trainers is that intensive simultaneous training for muscle strength and cardiovascular endurance is counterproductive. To test this premise, 14 healthy, untrained men trained four days per week for 20 weeks on a bicycle ergometer for endurance (END Group, n = 4), on an isokinetic device for increased torque production (ITP Group, n = 5), or on both devices (COMBO Group, n = 5). The ITP and COMBO groups had equal torque gains throughout the study (234 +/- 45 and 232 +/- 23 N.m, respectively). After 11 weeks, both END and COMBO groups had similar gains in maximal oxygen consumption (VO2max) (in milliliters per kilogram of body weight per minute). During the last half of the study, however, the END Group had a significant gain in VO2max (p less than .05) of 4.7 +/- 1.2 mL.kg-1.min-1, whereas the COMBO Group had a nonsignificant gain (p greater than .05) of 1.8 +/- 0.6 mL.kg-1.min-1. In harmony with this finding, the END Group showed a significant increase (p less than .05) in citrate synthase activity (15.5 +/- 7.9 mumol.g-1.min-1), whereas the COMBO Group had no significant increase. The authors concluded that simultaneous training may inhibit the normal adaptation to either training program when performed alone. The extent of the interference probably depends on the nature and intensity of the individual training program. [Nelson AG, Arnall DA, Loy SF, et al: Consequences of combining strength and endurance training regimens.

Effects of prior strength exercise on the heart rate oxygen uptake relationship during submaximal exercise.

Fourteen young males (mean age 26.7 yrs) were tested to determine if there was an alteration, in the heart rate-oxygen uptake relationship during submaximal cycle ergometer exercise following isokinetic strength training activity as has been documented following high intensity endurance activity. Results indicated that there was a significant increase rate without a concomitant increase in heart oxygen uptake during the first five minutes of submaximal cycle riding at 73% VO2max after heavy strength leg exercise, angular velocity of 30 degrees/second, when compared to no prior exercise. This alteration in the heart rate-oxygen uptake relation is not apparent by 20 minutes of the same submaximal exercise despite higher lactate values and greater ratings of perceived exertion. For individuals using heart rate as a guide to exercise intensity, the elevated heart rate at five minutes of submaximal exercise following heavy strength leg exercise does not exceed the 20 minute value which is an accurate reflection of energy cost and intensity.

Physiological Responses to Hand-Carried Weights.

In brief: Thirty trained men carrying either nothing, 1-lb weights, or 5-lb weights in each hand were tested on a motorized treadmill. The purpose was to determine whether using hand-held weights elicits a pressor reflex, in which heart rate and BP rise disproportionately to oxygen consumption (VO2). VO2 was measured during walking and running to see if it changed in proportion to heart rate response. Both walking and running while carrying 5-lb weights produced significant increases in V2, but only walking produced significant differences in heart rate. The oxygen pulse (the amount of oxygen used per heart beat) was not different for any of the three treatments. The authors concluded that carrying weights in the hands can help increase the training intensity for walkers or joggers who cannot or do not wish to jog or run at a higher speed.