R. L. Hughson
University of Waterloo
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Cardiovascular Research | 1996
J. K. Shoemaker; Stuart M. Phillips; H. J. Green; R. L. Hughson
OBJECTIVE The hypothesis that the adaptation to endurance exercise training included a faster increase in blood flow at the onset of exercise was tested in 12 healthy young men who endurance-trained (ET) 2 h/day, for 10 days at 65% VO2 peak on a cycle ergometer, and in 11 non-training control (C) subjects. METHODS Blood flow was estimated from changes in femoral artery mean blood velocity (MBV) by pulsed Doppler. Beat-by-beat changes in cardiac output (CO) and mean arterial pressure (MAP) were obtained by impedance cardiography and a Finapres finger cuff, respectively. MBV, MAP and CO were measured at rest and during 5 min of dynamic knee extension exercise. Both legs worked alternately with 2 s raising and lowering a weight (15% maximal voluntary contraction) followed by 2 s rest while the other leg raised and lowered the weight. RESULTS In the ET group the time to 63% (T63%) of the approximately exponential increase in MBV following 10 days of training (8.6 +/- 1.2 s, mean +/- s.e.) was significantly faster than the Day 0 response (14.2 +/- 2.1 s, P < 0.05). The T63% of femoral artery vascular conductance (VCfa) was also faster following 10 days of ET (9.4 +/- 0.9 s) versus Day 0 (16.0 +/- 2.5 s) (0.05). There was no change in the T63% of both MBV and VCfa for the C group. The kinetics of CO were not significantly affected by ET, but the amplitude of CO in the adaptive phase, and at steady state, were significantly greater (P < 0.05) at Day 10 compared to Day 0 for the ET group with no change in the C group. CONCLUSIONS These data supported the hypothesis that endurance training resulted in faster adaptation of blood flow to exercising muscle, and further showed that this response occurred early in the training program.
Medicine and Science in Sports and Exercise | 1987
Farla L. Kaufman; R. L. Hughson; John P. Schaman
The effects of dynamic exercise on the acute recovery blood pressure (BP) were studied in normotensive and hypertensive subjects. Three groups [eight normotensives, age 19 to 29 yr (N1); eight normotensives, age 35 to 62 yr (N2); and eight hypertensives, age 44 to 57 yr (H)] were tested over three separate sessions. The first two sessions were for familiarization with the protocol and test procedures. Resting systolic BP decreased (P less than 0.01) in all groups from sessions 1 to 3: N1 = 126 to 121 mm Hg; N2 = 127 to 120; H = 155 to 142. Resting diastolic BP decreased (P less than 0.05) in the N1 and H groups from 77 to 73 and 98 to 95 mm Hg, respectively. On the third day, each subject followed the protocol of Wilcox et al. (8) of 15 min of seated rest, five 10-min periods of treadmill walking with a 3-min rest between each period, and 60 min of seated recovery. Exercise was performed at 67% of estimated maximal heart rate. In all three groups, significant (P less than 0.05) reductions in both systolic BP (N1 = -12 +/- 1; N2 = -10 +/- 2; H = -12 +/- 3) and diastolic BP (N1 = -5 +/- 2; N2 = -5 +/- 1; H = -7 +/- 2) occurred from pre-exercise rest to post-exercise rest. Systolic BP remained lower following 60-min recovery (P less than 0.02), while diastolic BP returned to pre-exercise levels in all three groups. No between-group differences were observed in the magnitude of reduction of BP post-exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
Medicine and Science in Sports and Exercise | 1990
R. L. Hughson
The rate of increase in oxygen uptake (VO2) at the onset of a step change in work rate can be studied to provide information about the physiological mechanisms that control this process. Several systems must interact to produce the total response. These can be grouped into oxygen transport and oxygen utilization mechanisms. In this paper, the hypothesis that one or the other of these mechanisms limits the adaptation of VO2 to a change in work rate will be examined. In addition to the traditional approach with step changes in work rate, the responses to other work rate forcing functions will be reported. These include ramp, impulse, and pseudorandom binary sequence work rate changes. The evidence that is accumulating from studies involving transitions from different baseline levels of exercise, as well as studies of the effects of hypoxia and beta-adrenergic receptor blockade, has led to the conclusion that oxygen transport mechanisms limit the rate of increase in VO2. However, the dynamic response of VO2 in the presence of adequate oxygen is not much different from that of oxygen limited conditions.
Medicine and Science in Sports and Exercise | 1982
R. L. Hughson; H. J. Green
The effect of work rate increase in ramp work tests was studied in six healthy subjects. Each subject exercised on a cycle ergometer with the work rate incremented by either 65.4 W . min-1 and 49.0 W . min-1 for the fast ramps or 8.2 W . min-1 and 6.1 W . min-1 for the slow ramps for male and female subjects, respectively. Gas exchange was monitored by open-circuit spirometry. Arterialized venous blood samples were obtained from a dorsal hand vein. The peak VO2 was not significantly different for fast (3218 +/- 602 ml . min-1, X +/- SD) and slow (3237 +/- 601 ml . min-1) ramp tests. Gas-exchange anaerobic threshold, determined by multi-segment linear regression of VE vs VO2, was similar for fast and slow ramp tests (1742 +/- 415 and 1925 +/- 639 ml O2 . min-1, P greater than 0.05). The VO2 at which blood lactate increased 0.5 mM above resting levels was lower (1463 +/- 259 ml . min-1, P less than 0.05) than the gas-exchange anaerobic threshold for the slow ramp test. The VO2 at which blood lactate reached 2.0 mM was greater (2383 +/- 247 ml . min-1, P less than 0.05) than the gas-exchange anaerobic threshold for the fast ramp test. In addition to these lactate differences, blood pH and HCO3- did not change in direct proportion to the lactate concentration in either test. Blood PCO2 was significantly (P less than 0.05) greater at the point of exhaustion in the fast ramp test (42.2 +/- 2.3 mmHg) than in the slow ramp test (26.7 +/- 2.1 mmHg). It is concluded that the gas-exchange anaerobic threshold can be clearly dissociated from the blood lactate threshold by altering the work rate forcing function. Other mechanisms, such as H+ efflux and CO2 storage capacity, are more likely explanations for the gas-exchange anaerobic threshold.
Cardiovascular Research | 1997
J. K. Shoemaker; M.J MacDonald; R. L. Hughson
OBJECTIVE Whether the dimensions of conduit arteries contribute to the time course of change in blood flow during voluntary rhythmic exercise, and the mechanisms governing such a response in humans, are not known. METHODS The time course of change in the vascular and blood flow dynamics in the brachial artery during the transition between rest and 5 min of rhythmic handgrip exercise was assessed in humans using continuous measures of brachial artery mean blood velocity (MBV; pulsed Doppler), diameter (echo Doppler) and mean arterial pressure (Finapres). The exercise cadence was 1s/1s (Fast) and 1s/2s (Slow) work/rest schedules while supine with the arm positioned above or below the heart. RESULTS Brachial artery diameter of the active arm was reduced 5% at approximately 10 s following the onset of exercise performed above the heart (P < 0.05), irrespective of work rate, and returned to rest levels by 30 s with no concurrent changes in arterial pressure. By 2 min of the Fast contraction rate exercise, brachial artery diameter of the active arm was greater than rest (P < 0.05) irrespective of arm position. Brachial artery dimensions in the contralateral inactive arm were not altered during exercise (P > 0.05). Compared with rest, MBV and forearm blood flow at 5 s of exercise were increased in the active arm but were reduced transiently in the inactive limb (P < 0.05). CONCLUSIONS Conduit artery responses to exercise were dependent upon the work rate and arm position. The delayed dilation in the heavier exercise, independent of arm position, suggests that stimuli related to the metabolic activity of the distal active skeletal muscle may influence the dimensions of the conduit artery.
Medicine and Science in Sports and Exercise | 1987
H. J. Green; Laurie L. Jones; R. L. Hughson; Doug C. Painter; B. W. Farrance
To investigate the effect of training-induced increases in plasma volume on maximal aerobic power, 8 male subjects (age 19 to 24 yr) underwent a 4-d training program (2 h X d-1) at an estimated 71% maximal aerobic power. Following training, plasma volume measured using 131I-human serum albumin increased by 20.3% (P less than 0.01) whereas red cell volume remained unchanged and total blood volume increased by 12.3% (P less than 0.01). During progressive sub-maximal cycle exercise, oxygen consumption, carbon dioxide production, ventilation, and blood lactate concentration remained unchanged following the training whereas heart rate was significantly elevated (P less than 0.05). Significant post-training elevations were also noted in carbon dioxide production (P less than 0.05), blood lactate (P less than 0.01), and peak power output (P less than 0.05) during maximal exercise. Maximal aerobic power and ventilation were not altered. It is concluded that hypervolemia induced by short-term exercise training does not affect oxygen consumption either during sub-maximal or maximal exercise.
Archive | 1996
R. L. Hughson; H. J. Green; Stuart M. Phillips; J. K. Shoemaker
Endurance performance is dependent on the coordinated responses of the cardiovascular and respiratory systems, muscle metabolism, mechanical efficiency, and thermoregulation. A number of reviews have focused on one, or several, aspects of these responses (1,7,18). Yet, one central tenet of optimizing endurance performance revolves around the efficient aerobic transformation of metabolic substrate into mechanical power output, with delayed depletion of the glycogen reserves (1,10). Thus, it is important to have an efficient oxygen transport system and a metabolic system that supplies appropriate substrates to the mitochondria for oxidative metabolism with minimal concurrent glycolysis, a concept called “tight coupling” of oxidative metabolism (14).
Journal of Applied Physiology | 1983
H. J. Green; R. L. Hughson; G. W. Orr; D. Ranney
Journal of Applied Physiology | 1995
Stuart M. Phillips; H. J. Green; Maureen J. MacDonald; R. L. Hughson
Journal of Applied Physiology | 1982
G. W. Orr; H. J. Green; R. L. Hughson; G. W. Bennett