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B F Hurley

Publications and source records attributed to B F Hurley.

62 records · Page 4Linked to original sources

Endurance training in older men and women II. Blood lactate response to submaximal exercise.

Seven men and four women (age 63 +/- 2 yr, mean +/- SD, range 61-67 yr) participated in a 12-mo endurance training program to determine the effects of low-intensity (LI) and high-intensity (HI) training on the blood lactate response to submaximal exercise in older individuals. Maximal oxygen uptake (VO2max), blood lactate, O2 uptake (VO2), heart rate (HR), ventilation (VE), and respiratory exchange ratio (R) during three submaximal exercise bouts (65-90% VO2max) were determined before training, after 6 mo of LI training, and after an additional 6 mo of HI training. VO2max (ml X kg-1 X min-1) was increased 12% after LI training (P less than 0.05), while HI training induced a further increase of 18% (P less than 0.01). Lactate, HR, VE, and R were significantly lower (P less than 0.05) at the same absolute work rates after LI training, while HI training induced further but smaller reductions in these parameters (P greater than 0.05). In general, at the same relative work rates (ie., % of VO2max) after training, lactate was lower or unchanged, HR and R were unchanged, and VO2 and VE were higher. These findings indicate that LI training in older individuals results in adaptations in the response to submaximal exercise that are similar to those observed in younger populations and that additional higher intensity training results in further but less-marked changes.

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Effects of high-intensity strength training on cardiovascular function.

Thirteen healthy, untrained males (age 44 +/- 1 yr, range 40-55 yr) were studied to determine the effects of 16 wk of high-intensity, variable-resistance, Nautilus strength training on cardiovascular function. A control group consisting of 10 untrained males (age 52 +/- 2 yr, range 40-64 yr) underwent the same evaluation procedures as the training group. Maximal oxygen uptake (VO2max), cardiac output during submaximal exercise, and body composition were determined before and after training. In addition, the physiological responses to an acute training session were evaluated. Muscular strength increased markedly, as evidenced by a 44% average increase in the "one-repetition maximum" in the various exercises. Body weight and percent body fat did not change with training, though fat-free weight did increase (66.9 +/- 2.6 vs 68.8 +/- 2.7 kg, P less than 0.05) significantly. Maximal oxygen uptake did not change significantly in either the training or the control group, and there were no changes in the hemodynamic responses to submaximal exercise after training. These findings indicate, therefore, that high-intensity, variable-resistance strength training produces no adaptative improvement in cardiovascular function. The physiological responses measured during a training session provide evidence that this lack of cardiovascular adaptation may be due to the low percentage of VO2max elicited by this form of exercise.

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Failure of endurance training to alter the cardiovascular response to static contraction.

The purpose of this study was to determine whether endurance training alters the cardiovascular response to static contractions of the trained, but not untrained, musculature. Six healthy, untrained males (aged 23-36 years) underwent 10-12 weeks of intensive training involving both cycling and running. Peak VO2 on the bicycle ergometer, VO2max during graded treadmill running and concentrations of citrate synthase (CS) and malate dehydrogenase (MDH) in the vastus lateralis muscle were measured before and after training. Subjects performed static leg extension and forearm extension at 30% of maximal voluntary contraction until exhaustion before and after training. Heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressure were measured at rest, and in addition to perceived exertion (PE), every 30 s during contraction. Endurance training elicited significant increases in peak VO2 (36%), VO2max (32%), CS (25%) and MDH (42%) (all P less than 0.05). HR at rest was significantly lower (P less than 0.05) after training, while SBP and DBP were unchanged. HR, SBP, DBP and PE increased throughout both types of static contractions. However, the magnitude of the increases were unaffected by training. In contrast to recent findings, these results suggest that the increases in heart rate and blood pressure in response to static contraction are not altered after endurance training in either the trained or the untrained muscle groups.

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Carbohydrate feeding during prolonged strenuous exercise can delay fatigue.

This study was undertaken to determine whether carbohydrate feeding during exercise can delay the development of fatigue. Ten trained cyclists performed two bicycle ergometer exercise tests 1 wk apart. The initial work rate required 74 +/- 2% of maximum O2 consumption (VO2 max) (range 70-79% of VO2 max). The point of fatigue was defined as the time at which the exercise intensity the subjects could maintain decreased below their initial work rate by 10% of VO2 max. During one exercise test the subjects were fed a glucose polymer solution beginning 20 min after the onset of exercise; during the other they were given a placebo. Blood glucose concentration was 20-40% higher during the exercise after carbohydrate ingestion than during the exercise without carbohydrate feeding. The exercise-induced decrease in plasma insulin was prevented by carbohydrate feeding. The respiratory exchange ratio was unchanged by the glucose feeding. Fatigue was postponed by carbohydrate feeding in 7 of the 10 subjects. This effect appeared to be mediated by prevention of hypoglycemia in only two subjects. The exercise time to fatigue for the 10 subjects averaged 134 +/- 6 min (mean +/- SE) without and 157 +/- 5 min with carbohydrate feeding (P less than 0.01).

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The effects of rest and exercise in the cold on substrate mobilization and utilization.

The effects of altering skin and core temperature by cold exposure and exercise on substrate mobilization and utilization were examined. Six subjects between the ages of 22-27 years rested and exercised in neutral and cold environments to produce 1) a neutral core and neutral skin temperature, 2) a neutral core and cold skin temperature, and 3) a cold core and cold skin temperature. Free fatty acid (FFA), glucose (GL), Lactate (LA), hemoglobin (Hb), and hematocrit (Hct) concentrations were measured along with heart rate (HR), respiratory exchange ratio (R) and oxygen consumption (VO2) after 30, 60, and 90 min of exposure to each condition. FFA, GL, LA, Hb, and Hct concentrations increased significantly during rest when both mean skin temperature (Tsk) and rectal temperature (Tre) were reduced. Plasma FFA concentration was also significantly elevated and R values were reduced during exercise when both Tsk and Tre were lowered compared to exercise in a neutral environment. No significant differences in substrate concentration, hemoconcentration, or R values were observed when Tsk alone was reduced at rest or during exercise. It is concluded that a preferential utilization of fat occurs during exercise in the cold when both Tsk and Tre are reduced compared to exercise in a neutral environment.

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Cardiovascular and sympathetic reactions to in-flight emergency responses among base fire fighters.

The responses of 12 healthy male fire fighters to simulated and actual in-flight emergencies were investigated. Subjects were aroused from sleep during all emergency responses. The ECG, blood pressure, heart rate (HR), rate-pressure product (RPP), and plasma norepinephrine (NE) responses were determined. Despite a mean HR increase of 112% (75 beats/min) and a 145% rise in RPP, there was no significant elevation in plasma NE concentration during the emergency response. Legible ECG tracings showed no abnormal ST segment deviations or arrhythmias. The HR, BP, and RPP results indicated a greater cardiovascular response to emergencies among inactive fire fighters than among those who were physically active. Based on the observed differences between emergency and simulated emergency responses, we concluded that the physiological reactions during emergency responses were due primarily to the arousal response. When suddenly aroused from sleep, the fire fighter's response to in-flight emergencies produces significant elevations in HR and myocardial oxygen consumption which were unrelated to increases in sympathetic activity.

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Resistance training alters cytokine gene expression in skeletal muscle of adults with type 2 diabetes.

Resistance training results in muscle hypertrophy and improves glycemic control in patients with type 2 diabetes. Whether resistance training modulates inflammation in muscles of diabetic patients remains unknown. We examined the expression of genes encoding the cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and transforming growth factor-beta1 (TGF-beta1) as well as the pan-leukocyte marker CD18. Thirty men and women (67+/-7 years) were randomized to either 16 weeks of resistance training and usual diabetes care (EX) or to usual diabetes care only (CON). Muscle biopsies were obtained from the vastus lateralis muscle prior to the 16-week intervention, and 72 h following the maximal strength test post-intervention. Fiber cross-sectional area (CSA) was determined following ATPase staining. Cytokine and CD18 transcript levels were assessed by real-time PCR. Resistance training increased CSA of type I and II fibers (both P <0.05) and IL-1beta transcript levels (P = 0.05). TNF-alpha (P<0.05) and TGF-beta1 transcripts (P<0.05) increased over time in the EX group, but these increases did not differ from those in the CON group. In both groups, the increase in CD18 transcripts remained minimal. The two groups differ by the relationship between changes in CD18 and changes in cytokine transcripts, suggesting that resistance training affects the source of cytokines in muscle. Our studies establish that resistance training in older adults with type 2 diabetes results in muscle fiber hypertrophy, despite a greater accumulation of inflammatory cytokine transcripts in muscle.

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