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PubMed1977

Central and regional circulatory effects of adding arm exercise to leg exercise.

7 young, healthy, male subjects performed exercise on bicycle ergometers in two 20 min periods with an interval of 1 h. The first 10 min of each 20 min period consisted of arm exercise (38--62% of Vo2 max for arm exercise) or leg exercise (58--78% of Vo2 max for leg exercise). During the last 10 min the subjects performed combined arm and leg exercise (71--83% of Vo2 max for this type of exercise). The following variables were measured during each type of exercise: oxygen uptake, heart rate, mean arterial blood pressure, cardiac output, leg blood flow (only during leg exercise and combined exercise), arterio-venous concentration differences for O2 and lactate at the levels of the axillary and the external iliac vessels. Superimposing a sufficiently strenuous arm exercise (oxygen uptake for arm exercise greater than 40% of oxygen uptake for combined exercise) on leg exercise caused a reduction in blood flow and oxygen uptake in the exercising legs with unchanged mean arterial blood pressure. Superimposing leg exercise on arm exercise caused a decrease in mean arterial blood pressure and an increased axillary arterio-venous oxygen difference. These findings indicate that the oxygen supply to one large group of exercising muscles may be limited by vasoconstriction or by a fall in arterial pressure, when another large group of muscles is exercising simultaneously.

Adult↗

PubMed1998

Attenuation of myocardial ischemia with repeated exercise in subjects with chronic stable angina: relation to myocardial contractility, intensity of exercise and the adenosine triphosphate-sensitive potassium channel.

OBJECTIVES: This study characterized the attenuation of myocardial ischemia observed with re-exercise to determine whether: 1) a differing exercise intensity modifies this attenuation; 2) it could be explained by contractile down-regulation or stunning; 3) it is mediated by activation of ATP-sensitive potassium channels (K+-ATP). BACKGROUND: Subjects with ischemic heart disease (IHD) frequently note less angina with re-exercise after a brief rest. Potential mechanisms of this 'warm-up' phenomenon have been little explored. METHODS: IHD subjects with a positive exercise test were studied. Groups I and II (12 subjects each) underwent 2 successive Naughton protocol exercise echocardiography tests (with 1 min instead of 2 min stages for Group II). Group D (10 subjects) had type II diabetes, were on > or =10 mg daily of the K+-ATP blocker, glibenclamide, and underwent the group I exercise protocol. The ischemic threshold or rate-pressure product at 1 mm ST segment depression, ST depression corresponding to the peak rate-pressure product of the first exercise (maximum ST depression equivalent), and left ventricular wall motion indexes before and immediately after each exercise were analyzed. RESULTS: Exercise-induced myocardial ischemia with re-exercise was similarly attenuated in groups I, II, and D. The ischemic threshold was raised by nearly 20% with re-exercise (p=0.001, p=0.02, and p=0.02, respectively) and the maximum ST depression equivalent was nearly halved on re-exercise (p=0.005, p=0.006, and p=0.001, respectively). Exercise-induced wall motion dysfunction was attenuated with re-exercise. In group I, wall motion returned to the initial baseline score prior to exercise 2, whereas in the more intense protocol of group II, wall motion dysfunction persisted prior to exercise 2. CONCLUSIONS: Thus, the attenuation of myocardial ischemia observed with re-exercise appears to be independent of the intensity of the exercise protocol and is not explained by down-regulation of myocardial contractility induced by the initial ischemic stimulus. Since results were similar in diabetic subjects on robust doses of glibenclamide, this phenomenon does not appear to be mediated by K+-ATP activation.

Adenosine Triphosphate↗

PubMed2004

How rheumatologists and patients with rheumatoid arthritis discuss exercise and the influence of discussions on exercise prescriptions.

OBJECTIVE: To describe how patients and their rheumatologists discuss exercise, and to identify predictors of exercise prescriptions. METHODS: Twenty-five rheumatologists and 132 patients with rheumatoid arthritis completed questionnaires and were audiotaped during a subsequent clinic visit. Chi-square and t-tests assessed associations between variables. Principal components analysis identified patterns of talk about exercise. Multivariate logistic regression identified predictors of an exercise prescription. RESULTS: Seventy of the 132 patients (53%) discussed exercise. Of these, 18 (26%) received an exercise prescription. Principal components analysis identified 3 patterns of talk about exercise. Aerobic exercise discussions contained more information about drawbacks, side effects, pain, and bargaining than did discussions about general exercises, and referral to physical therapy for exercise. Significant predictors of a prescription included rheumatologist-initiated discussion about exercise (odds ratio [OR] 4.6; P = 0.03); talk about exercise in improving function, exercise instructions, opinions about the usefulness of exercise (OR 3.1; P = 0.01); and discussions about non-exercise treatments (OR 1.6; P = 0.01). CONCLUSION: Exercise and referral to physical therapy for exercise are discussed differently and are 4 times more likely to occur when the rheumatologist initiates the discussion. These discussions strongly impact on the likelihood a patient receives an exercise prescription.

Adult↗

PubMed1998

Post-exercise changes in blood pressure, heart rate and rate pressure product at different exercise intensities in normotensive humans.

To evaluate the effect of exercise intensity on post-exercise cardiovascular responses, 12 young normotensive subjects performed in a randomized order three cycle ergometer exercise bouts of 45 min at 30, 50 and 80% of VO2peak, and 12 subjects rested for 45 min in a non-exercise control trial. Blood pressure (BP) and heart rate (HR) were measured for 20 min prior to exercise (baseline) and at intervals of 5 to 30 (R5-30), 35 to 60 (R35-60) and 65 to 90 (R65-90) min after exercise. Systolic, mean, and diastolic BP after exercise were significantly lower than baseline, and there was no difference between the three exercise intensities. After exercise at 30% of VO2peak, HR was significantly decreased at R35-60 and R65-90. In contrast, after exercise at 50 and 80% of VO2peak, HR was significantly increased at R5-30 and R35-60, respectively. Exercise at 30% of VO2peak significantly decreased rate pressure (RP) product (RP = HR x systolic BP) during the entire recovery period (baseline = 7930 +/- 314 vs R5-30 = 7150 +/- 326, R35-60 = 6794 +/- 349, and R65-90 = 6628 +/- 311, P < 0.05), while exercise at 50% of VO2peak caused no change, and exercise at 80% of VO2peak produced a significant increase at R5-30 (7468 +/- 267 vs 9818 +/- 366, P < 0.05) and no change at R35-60 or R65-90. Cardiovascular responses were not altered during the control trial. In conclusion, varying exercise intensity from 30 to 80% of VO2peak in young normotensive humans did not influence the magnitude of post-exercise hypotension. However, in contrast to exercise at 50 and 80% of VO2peak, exercise at 30% of VO2peak decreased post-exercise HR and RP.

Adult↗

PubMed2005

Pacific women's decisions about exercise adoption: utilising the stage-of-exercise-adoption model.

AIMS: To analyse the exercise patterns of Pacific women utilising the stage-of-exercise-adoption model, and to investigate how the pros and cons of exercising, exercise self-efficacy, self-reported health, and sociodemographic barriers to exercise influence exercise adoption. METHODS: A non-random questionnaire survey of 106 Pacific women living in the North Island of New Zealand. RESULTS: Thirty percent of the sample was sedentary, 34% were participating in some exercise, and 35% were exercising regularly. The balance between pros and cons of exercise, exercise self-efficacy, self-rated health and levels of barriers reliably differentiated respondents at extreme stages of exercise adoption. In addition, two specific barriers to exercise (not having friends who exercise, and being unsatisfied with current income) were associated with reduced exercise self-efficacy. CONCLUSIONS: A large number of Pacific women are sedentary, but analysis of the factors associated with exercise adoption level and exercise-related self-confidence provides a platform for future intervention. Exercise adoption interventions tailored specifically to Pacific women should focus on broader community-based systems that include peer-group participation, and emphasise inexpensive options for exercise.

Adult↗

PubMed1997

The effect of ambient temperature and exercise intensity on post-exercise thermal homeostasis.

We have previously demonstrated a prolonged (65 min or longer) elevated plateau of esophageal temperature (T(es)) (0.5-0.6 degrees C above pre-exercise values) in humans following heavy dynamic exercise (70% maximal oxygen consumption, VO2max) at a thermoneutral temperature (T(a)) of 29 degrees C. The elevated T(es) value was equal to the threshold T(es) at which active skin vasodilation was initiated during exercise (Th(dil)). A subsequent observation. i.e., that successive exercise/recovery cycles (performed at progressively increasing pre-exercise T(es) levels) produced parallel increases of Th(dil) and the post-exercise T(es), further supports a physiological relationship between these two variables. However, since all of these tests have been conducted at the same T(a) (29 degrees C) and exercise intensity (70% VO2max) it is possible that the relationship is limited to a narrow range of T(a)/exercise intensity conditions. Therefore, five male subjects completed 18 min of treadmill exercise followed by 20 min of recovery in the following T(a)/exercise intensity conditions: (1) cool with light exercise, T(a) = 20 degrees C, 45% VO2max (CL); (2) temperature with heavy exercise, T(a) = 24 degrees C, 75% VO2max (TH); (3) warm with heavy exercise, T(a) = 29 degrees C, 75% VO2max (WH); and (4) hot with light exercise, T(a) = 40 degrees C, 45% VO2max (HL). An abrupt decrease in the forearm-to-finger temperature gradient (T(fa) - T(fi)) was used to identify the Th(dil) during exercise. Mean pre-exercise T(es) values were 36.80, 36.60, 36.72, and 37.20 degrees C for CL, TH, WH, and HL conditions respectively. T(es) increased during exercise, and end post-exercise fell to stable values of 37.13, 37.19, 37.29, and 37.55 degrees C for CL, TH, WH, and HL trials respectively. Each plateau value was significantly higher than pre-exercise values (P < 0.05). Correspondingly, Th(dil) values (i.e., 37.20, 37.23, 37.37, and 37.48 degrees C for CL, TH, WH, and HL) were comparable to the post-exercise T(es) values for each condition. The relationship between Th(dil) and post-exercise T(es) remained intact in all T(a)/exercise intensity conditions, providing further evidence that the relationship between these two variables is physiological and not coincidental.

Adult↗

PubMed1994

Different effects of strenuous exercise and moderate exercise on platelet function in men.

BACKGROUND: Platelets play an important role in the pathogenesis of cardiovascular diseases. It is also noticed that on one hand, regular exercise can reduce the risk of cardiovascular diseases, and on the other hand, vigorous exercise provokes sudden cardiac death. We therefore hypothesize that various intensities of exercise may affect platelet function differently. METHODS AND RESULTS: Strenuous and moderate exercise (about 50% to 55% of peak oxygen consumption, VO2peak) on a bicycle ergometer in 10 sedentary and 10 physically active healthy young men was executed on two separate occasions. Blood samples were collected before and immediately after exercise. A newly designed tapered parallel plate chamber was used to assess platelet adhesiveness. Platelet aggregation induced by ADP was evaluated by the percentage of reduction in single platelet count. beta-Thromboglobulin (beta-TG) and platelet factor 4 (PF4) were measured by ELISA. In addition, a similar study on 5 patients with stable angina were also conducted. Our results showed that (1) in the sedentary healthy group, platelet adhesiveness and aggregation were increased by strenuous exercise and depressed by moderate exercise; (2) in the active healthy group, platelet adhesiveness and aggregation were enhanced by severe exercise, whereas only aggregation was decreased by moderate exercise; (3) in the patients with stable angina, platelet adhesiveness and aggregation were enhanced by strenuous exercise and adhesiveness was suppressed by moderate exercise; (4) the degree of hemoconcentration induced by acute exercise tended to be related to the severity of exercise in all subjects; and (5) although severe exercise elevated beta-TG and PF4, there were no significant changes in beta-TG, PF4, and the ratio of beta-TG to PF4 in healthy subjects after exercise. CONCLUSIONS: It is concluded that platelet adhesiveness and aggregability may be sensitized by strenuous exercise in both healthy subjects and patients with stable angina. In contrast, platelet function can be suppressed significantly by moderate exercise in the healthy and tends to be depressed in patients with stable angina. The former may increase the risk of cardiac arrest and the latter may protect us from cardiovascular diseases. In addition, the effects of acute exercise tend to be more pronounced in the sedentary than in the active.

Adult↗

PubMed1999

The effects of exercise intensity on post exercise hypotension.

Ten normotensive, recreationally active participants aged 35.0 +/- 16.3 years, volunteered to participate in the study. Average baseline blood pressure (BP) was 132/75 mm Hg for systolic (SBP) and diastolic (DBP) pressure respectively. On two separate days, participants underwent testing in a randomised, repeated measures fashion such that they performed 30-min bouts of cycle ergometry at a power output which elicited 50 or 75% of VO2 Peak. Blood pressure was monitored continuously throughout the session by the Finapres method with 2-min windows recorded at rest, 5, 10, 15, 30, 45 and 60 min post exercise. SBP was similar between the two trials and became hypotensive at 5 through 15 min post exercise. The largest decrement (8 mm Hg) in SBP occurred 5 min post exercise. DBP was also unaffected by the intensity of exercise and was lower than before exercise at 5 and 15 through 45 min post exercise. Similarly, mean arterial pressure (MAP) showed significant decrements at 5 and 15 through 45 min post exercise irrespective of exercise intensity. Heart rate was greater during the 75% intensity than during the 50% intensity trial. Pre-exercise values were re-established by 45 min post exercise. VO2 remained significantly elevated above pre-exercise values in both trials until 15 min post exercise. Haematocrit increased significantly during both exercise bouts but returned to pre-exercise values by 10 min post exercise. This study indicates that cycle ergometry at 50 and 75% of VO2 Peak elicit similar reductions in post exercise BP. Therefore bouts of mild to moderate intensity exercise may be beneficial in the control of hypertension.

Adult↗

PubMed2005

Post-exercise palpation of pulse rates: its applicability to habitual exercisers.

Despite the increased popularity of heart rate (HR) monitors, endurance-trained adults as well as habitual exercisers often use pulse rate palpation to periodically monitor exercise intensity. However, due to the rapid recovery of HR following exercise bouts, post-exercise palpation of pulse rates may underestimate exercise HR. To test this hypothesis, we studied 20 young physically active adults performing two sets of exercise for 5 min at 70% and 85% of maximal HR on the treadmill; one with carotid and another with radial pulse count. Post-exercise palpation of pulse rate was lower (P < 0.01) than the actual HR during exercise, underestimating exercise HR by 20-27 bpm (beats per min). Even when ECG tracings of HR were analyzed immediately after exercise (0-15 s), a significant underestimation of exercise HR (7-9 bpm) still persisted (P < 0.05). Following exercise, pulse rate obtained by carotid palpation at both intensities and radial palpation at the lower intensity was no different from the corresponding HR measured with ECG. In the radial artery trial at the higher exercise intensity, pulse rate following exercise was lower (10 bpm; P < 0.05) than ECG-derived HR. Arterial stiffness, which is closely associated with arterial baroreflex sensitivity, was not significantly related to the changes in HR with carotid palpation. We concluded that post-exercise pulse palpations may not be appropriate as an indicator of exercise intensity in habitual exercisers.

Adolescent↗

PubMed2002

Low intensity exercise in humans accelerates mitochondrial ATP production and pulmonary oxygen kinetics during subsequent more intense exercise.

We undertook this study to determine whether low intensity exercise (55 % (O2,max) would significantly alter the metabolic and ventilatory responses observed during 10 min of subsequent moderate intensity exercise (75 % (O2,max). By executing this work, we hoped to further our understanding of the mechanisms that limit mitochondrial ATP production at the onset of exercise. Seven healthy human subjects performed 10 min of moderate intensity exercise in the presence and absence of 10 min of low intensity exercise, which preceded the moderate intensity exercise by 3 min. Muscle biopsy samples were obtained from the vastus lateralis at pre-determined time points and oxygen consumption kinetics were determined at rest and during low and moderate intensity exercise. Following low intensity exercise and 3 min of passive recovery, muscle lactate and acetylcarnitine concentrations were elevated above basal levels, but (O2) had returned to the resting rate. When moderate intensity exercise was preceded by low intensity exercise, there was a significant sparing of phosphocreatine (PCr, approximately 25 %, P < 0.05) and reductions in glucose 6-phosphate (G-6-P, approximately 50 %, P < 0.05) and lactate (approximately 50 %, P < 0.05) accumulation during the first minute of moderate intensity exercise. No differences were observed after 10 min of moderate intensity exercise. The (O2) on-kinetic response over the first minute of moderate intensity exercise was accelerated when preceded by low intensity exercise. Collectively, our results suggest the lag in the oxidative ATP delivery at the onset of moderate intensity exercise can be overcome by prior low intensity exercise. Furthermore, our findings support the view that this lag is at least in part attributable to a limitation in acetyl group delivery/availability at the onset of exercise, rather than delayed oxygen supply.

Adenosine Triphosphate↗

PubMed1997

The relationship between maximal expiratory flow and increases of maximal exercise capacity with exercise training.

We previously reported that patients with mild to moderate airflow limitation have a lower exercise capacity than age-matched controls with normal lung function, but the mechanism of this reduction remains unclear (1). Although the reduced exercise capacity appeared consistent with deconditioning, the patients had altered breathing mechanics during exercise, which raised the possibility that the reduced exercise capacity and the altered breathing mechanics may have been causally related. Reversal of reduced exercise capacity by an adequate exercise training program is generally accepted as evidence of deconditioning as the cause of the reduced exercise capacity. We studied 11 asymptomatic volunteer subjects (58 +/- 8 yr of age [mean +/- SD]) selected to have a range of lung function (FEV1 from 61 to 114% predicted, with a mean of 90 +/- 18% predicted). Only one subject had an FEV1 of less than 70% predicted. Gas exchange and lung mechanics were measured during both steady-state and maximal exercise before and after training for 30 min/d on 3 d/wk for 10 wk, beginning at the steady-state workload previously determined to be the maximum steady-state exercise level that subjects could sustain for 30 min without exceeding 90% of their observed maximal heart rate (HR). The training workload was increased if the subject's HR decreased during the training period. After 10 wk, subjects performed another steady-state exercise test at the initial pretraining level, and another maximal exercise test. HR decreased significantly between the first and second steady-state exercise tests (p < 0.05), and maximal oxygen uptake (VO2max) and ventilation increased significantly (p < 0.05) during the incremental test, indicating a training effect. However, the training effect did not occur in all subjects. Relationships between exercise parameters and lung function were examined by regression against FEV1 expressed as percent predicted. There was a significant positive correlation between VO2max percent predicted and FEV1 percent predicted (p < 0.02), and a negative correlation between FEV1 and end-expiratory lung volume (EELV) at maximal exercise (p < 0.03). There was no significant correlation between FEV1 and maximal HR achieved during exercise; moreover, all subjects achieved a maximal HR in excess of 80% predicted, suggesting a cardiovascular limitation to exercise. These data do not support the hypothesis that the lower initial VO2max in the subjects with a reduced FEV1 was due to deconditioning. Although increased EELV at maximal exercise, reduced VO2max and a reduced VO2max response with training are all statistically associated with a reduced FEV1, there is no direct evidence of causality.

Case-Control Studies↗

PubMedDate not supplied

Noninvasive ventilation during exercise training improves exercise tolerance in patients with chronic obstructive pulmonary disease.

PURPOSE: In patients with chronic obstructive pulmonary disease, pulmonary rehabilitation has been demonstrated to increase exercise capacity and reduce dyspnea. In the most disabled patients, the intensity of exercise during the training sessions is limited by ventilatory pump capacity. This study therefore evaluated the beneficial effect of noninvasive ventilation (NIV) support during the rehabilitation sessions on exercise tolerance. METHODS: This study included 14 patients with stabilized chronic obstructive pulmonary disease, ages 63 +/- 7 years, with a forced expiratory volume in 1 second (FEV(1)) 31.5% +/- 9.2% of predicted value. All 14 patients participated in an outpatient pulmonary rehabilitation program. Seven of the patients trained with NIV during the exercise sessions (NIV group), whereas the remaining seven patients breathed spontaneously (control group). Exercise tolerance was evaluated during an incremental exercise test and during constant work rate exercise at 75% of peak oxygen consumption (VO(2)) before and after the training program. RESULTS: The application of noninvasive ventilation increased exercise tolerance, reduced dyspnea, and prevented exercise-induced oxygen desaturation both before and after training. The pressure support was well tolerated by all the patients during the course of the training program. In the NIV group, training induced a greater improvement in peak VO(2) (18% vs 2%; P <.05) and a reduced ventilatory requirement for maximal exercise, as compared with the control group. The constant work rate exercise duration increased similarly in both groups (116% vs 81%, nonsignificant difference), and posttraining blood lactate was decreased at isotime (P <.05 in both groups), but not at the end of the exercise. CONCLUSION: In this pilot study, exercise training with noninvasive ventilation support was well tolerated and yielded further improvement in the increased exercise tolerance brought about by pulmonary rehabilitation in patients with chronic obstructive pulmonary disease. This improved exercise tolerance is partly explained by a better ventilatory adaptation during exercise.

Aged↗

PubMed1991

Non-exercising muscle metabolism during exercise.

Glycogen decrements have been observed in non-exercising muscles during exercise. We therefore investigated whether the degraded glycogen was retained within the muscle in the form of glycolytic intermediates, or whether it was effluxed from the non-exercising muscles. For these studies a suspension harness was used to unload the hindlimb muscles at rest and during exercise [McDermott et al. (1987) J Appl Physiol 63:1275-1283]. Concentrations of glycogen and glycolytic intermediates glucose 6-phosphate, fructose 6-phosphate, fructose 1,6-bisphosphate, glycerol 3-phosphate, and lactate) were measured in non-exercising and exercising muscles (soleus, plantaris, red and white gastrocnemius) during a 90-min exercise about 15 m/min, 8% grade). On-line electromyographic analysis showed that the contractile activity in the non-exercising muscles was markedly lower than in the exercising muscles. Similar decrements in muscle glycogen levels were observed in both the non-exercising and exercising muscles at the end of the 90-min, exercise bout (P less than 0.05), despite significantly different activity profiles. An increase in tissue lactate concentrations occurred in both non-exercising and exercising muscle (P less than 0.05), although only slight changes in the glycolytic intermediates occurred. The sum total of all the accumulated glycolytic intermediates and lactate (converted to glucosyl units) in the non-exercising muscles only accounted for a small fraction of the glycogen degraded (approximately 15%-28%). We conclude that the metabolism of glycogen is enhanced in non-exercising muscle, and that glycogen utilization is uncoupled from the energetic demands of the muscle. Furthermore, the glycogen mobilized in non-exercising muscle is not retained within the muscle in other metabolite pools.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1996

The effect of exercise duration on the fast component of exercise hyperpnoea at work rates below the first ventilatory threshold.

We examined the effect of exercise duration on the fast component of exercise hyperpnoea for light and moderate work rates [mean oxygen uptakes (SD) = 1.00 (0.27) 1.min-1 and 1.77 (0.53) 1.min-1, respectively]. Ten subjects exercised on a motor-driven treadmill while ventilation and end-expiratory partial pressures of carbon dioxide and oxygen were recorded on a breath-by-breath basis. The magnitude of the fast component of exercise hyperpnoea was determined by quantifying the abrupt changes in ventilation at the beginning and end of exercise. Five exercise tests with durations ranging from 1 min to 8 min were completed at each of the two periods of exercise at different work rates. Subsequent statistical analysis revealed that the rapid changes in ventilation at the end of exercise were significantly smaller than those at the start [pooled means (SE) = 6.27 (0.48) and 13.05 (1.06) 1.min-1 for light and moderate exercises respectively] regardless of exercise duration. Further statistical analysis failed to find a relationship between the fast ventilatory changes present at the end of exercise, expressed as a proportion of those at the start of exercise, and either exercise duration or work rate (73% and 62% for light and moderate exercises respectively). We conclude that the fast component of exercise hyperpnoea declines rapidly in the first minute of exercise, and interpret this decline as an indication that the fast neural drive to ventilation, proportional to limb movement frequency, adapts quickly at the start of exercise.

Adult↗

PubMed2004

High bone mass gained by exercise in growing male mice is increased by subsequent reduced exercise.

Exercise-induced bone gains are lost if exercise ceases. Therefore, continued exercise at a reduced frequency or intensity may be required to maintain these benefits. In this study, we evaluated whether 4 wk of reduced exercise after 4 wk of running exercise in growing male mice results in the maintenance of high bone mass. Five-week-old mice were divided into the following groups: 1) baseline control; 2) 4-wk control; 3) 4-wk exercise; 4) 8-wk control; 5) 4-wk exercise followed by 4-wk cessation of training; and 6) 4-wk exercise followed by reduced exercise at half the frequency. The regimen consisted of exercise 6 days/wk, and the reduced exercise regimen consisted of running 3 days/wk on a treadmill for 30 min/day, at 12 m/min on a 10 degrees uphill slope. Running exercise significantly increased bone mineral density of the femur, periosteal mineral apposition rate, bone formation rate, percent labeled perimeter at the midfemur, and osteogenic activity of bone marrow cells. However, these parameters declined to the age-matched sedentary control after cessation of training. In contrast, the reduced exercise group had significantly higher mineral apposition rate compared with those of the sedentary control and cessation of training groups. Furthermore, bone mineral density for the reduced exercise group was significantly higher than those for the other groups. These results suggest that the high bone formation gained through exercise can be maintained, and bone mass was further increased by subsequent exercise even if the exercise frequency is reduced.

Adaptation, Physiological↗

PubMed1996

Comparison of metabolic, ventilatory, and neurohumoral responses during light forearm isometric exercise and isotonic exercise in congestive heart failure.

Maximal treadmill exercise responses were compared with light forearm isometric exercise responses in patients with chronic, stable heart failure (n = 14), and normal sedentary controls (n = 11). Isometric exercise was performed to exhaustion with 25% of maximal voluntary contraction. Gas-exchange analysis was used to determine oxygen consumption (VO2), carbon dioxide production (VCO2), and minute ventilation (VE) during exercise. Significant correlations were observed in normal controls, but not in patients with heart failure, between peak isotonic exercise and peak isometric exercise for VO2 (r = 0.75, p = 0.001) and VCO2 (r = 0.67, p <0.03), and between submaximal isotonic exercise (50% of peak) and peak isometric exercise for VO2 (r = 0.75, p = 0.007), VCO2 (r = 0.67, p = 0.02), and VE (r = 0.71, p = 0.01). At 90 seconds after isometric exercise in both groups, significant correlations (p <0.05) were observed with peak isotonic exercise for VE (r = 0.62 normals, and r = 0.63 heart failure). Plasma norepinephrine increased significantly (p <0.01) after both isotonic and isometric exercise in patients with heart failure, although peak values were greater with isotonic than with isometric exercise (p = 0.01). Plasma atrial natriuretic peptide and renin activity did not change with either isotonic or isometric exercise. In conclusion, maximal isotonic exercise responses are not predictive of peak isometric VO2 or VCO2 in patients with heart failure. However, VE during maximal isotonic exercise predicts postisometric exercise ventilation in both normals and patients with heart failure; this may determine the extent of dyspnea that patients with heart failure experience with isometric activities of daily living.

Adult↗

PubMed2000

The effects of exercise duration on post-exercise hypotension.

STUDY 1: Thirteen normotensive participants with average baseline blood pressure of 126/71 mm Hg participated in the study. Participants performed bouts of cycle ergometry for 15, 30 and 45 min at 70% VO2 Peak. Blood pressure was monitored by the Finapres method with 2 min windows recorded at rest, 5, 10, 15, 30, 45 and 60 min post-exercise. Following exercise, systolic blood pressure (SBP) was similar between the three trials and was reduced from pre-exercise values at 5 through 60 min of measurement. Diastolic blood pressure (DBP) was also unaffected by the duration of exercise and was lower than before exercise at 30 through 45 min post-exercise. STUDY 2: Eight borderline hypertensive participants with average baseline blood pressure of 133/79 mm Hg participated in the study. Subjects performed bouts of cycle ergometry for 10 and 30 min at 70% VO2 Peak. Following exercise, blood pressure was monitored as in study 1. SBP was similar between both trials and was reduced from baseline at 5 through 60 min post-exercise. The largest decrement of SBP was 14 mm Hg and occurred 15 min post-exercise. DBP was also unaffected by the duration of exercise and was lower than pre-exercise levels at 5 min and again at 15 through 45 min post-exercise. Mean arterial pressure (MAP) also showed significant decrements throughout the entire 1 h post-exercise period by a maximum of 9 mm Hg at 15 min post-exercise, irrespective of exercise duration. We conclude that moderately intense exercise may be as brief as 10 min in duration in order to elicit a decrease in resting blood pressure and may have potential benefits as a non-pharmacological aid to hypertension.

Adult↗

PubMed1997

Dyspnoea and exercise intolerance during cardiopulmonary exercise testing in patients with univentricular heart. The effects of chronic hypoxaemia and Fontan procedure.

BACKGROUND: Patients with univentricular hearts have decreased exercise tolerance and may demonstrate exertional dyspnoea. It is not known if chronic hypoxaemia exacerbates exercise intolerance and contributes to symptomatic limitation. The extent to which surgical correction of a right-to-left shunt by a Fontan-type procedure can increase exercise tolerance by reducing arterial deoxygenation is not well documented. The cardiopulmonary exercise responses and the symptomatic status in two groups of univentricular patients, those who are cyanotic and those who are acyanotic with Fontan-type circulation, were compared. METHODS AND FINDINGS: Cardiopulmonary exercise testing was performed in 10 univentricular patients with rest or stress-induced cyanosis (age 30.5 +/- 2.3 [SE] years; 5 men) who had palliative or no surgery and eight patients (age 29.4 +/- 1.5 years; 4 men) with Fontan-type circulation. Peak oxygen consumption was comparable in both groups of univentricular patients (21.7 +/- 2.5 vs 21.0 +/- 1.9 ml.kg-1.min-1, P = 0.85) but was less than an age-matched group of 10 healthy subjects (34.7 +/- 1.9 ml.kg-1.min-1, P < 0.001 for both). Arterial oxygen saturation was 90.6% at rest in the cyanotic patients compared with 95.1% in the Fontan patients (P < 0.001) and at peak exercise, 66.2% compared with 90.5% (P < 0.001). Using a modified Borg scale (0-10), the symptoms of dyspnoea and fatigue were also assessed during exercise in the patient groups. The Borg scores for dyspnoea in the cyanotic and the corrected univentricular patients were, respectively, as follows: Stage 1: 0.5 vs 1.7; P= 0.04; Stage 2: 1.8 vs 2.3, P = 0.5; Stage 3: 3.0 vs 3.5, P = 0.7; Peak Exercise: 4.9 vs 4.8, P = 0.9. In addition, the Borg scores for fatigue were: Stage 1: 0.4 vs 1.6, P = 0.08; Stage 2: 2.0 vs 2.2, P = 0.9; Stage 3: 3.0 vs 4.3, P = 0.5; Peak Exercise: 4.9 vs 5.4, P = 0.5. The major limiting symptom at peak exercise was dyspnoea in four cyanotic patients compared with one in the Fontan group (Chi-square 0.982, P > 0.10). The arterial oxygen desaturation at peak exercise in the cyanotic patients limited by dyspnoea was not different from those limited by fatigue (67.5 +/- 10.1% vs 66.7 +/- 13.7%, P = 0.92). Exercise tolerance was also not related to the arterial oxygen saturation at peak exercise (r = 0.47, P = 0.17) in these patients. CONCLUSIONS: Despite correction with Fontan-type surgery, the exercise tolerance and symptoms of these univentricular patients remained similar to those who were cyanosed. Cyanotic patients have adjusted to chronic hypoxaemia and it does not appear to determine the exercise tolerance or the genesis of dyspnoea in these patients. Further randomized prospective studies are required to investigate the long-term benefits of Fontan-type procedures in these patients on exercise tolerance, symptoms and prognosis.

Adult↗