Sudden Strenuous Exercise Research Articles

The Effects of a Delay Following Warm-up on the Heart Rate Response to Sudden Strenuous Exercise

Introduction: Sudden strenuous exercise (SSE) has previously been shown to result in electrocardiograph (ECG) abnormalities indicative of myocardial ischemia when not preceded by a warm-up. Athletes regularly undergo SSE and are often unable to warm-up immediately prior to competition. It is unknown whether a delay post warm-up will result in the same heart rate (HR) response to SSE as seen with no warm-up. Aims: To compare the HR response and to observe for ECG abnormalities during SSE with a warm up, with a delay after warm up and without a warm up. Methods: Seven male subjects randomly completed three SSE exercise conditions while being monitored by ECG; a 15 second supramaximal sprint following three conditions: no warm up (NW); Original Research Article Lesser and Hodges; BJMMR, 8(9): 765-771, 2015; Article no.BJMMR.2015.504 766 immediately following a warm-up (WU); and following a 10-minute delay post warm up (D). There were no ECG abnormalities across any of the conditions indicative of myocardial ischemia. Results: Significant differences (p<0.05) were found in the HR response for all time periods during exercise between WU and NW, between WU and D, but not between D and NW. A delay between warm-up and SSE resulted in a lowered HR response to the SSE compared with a warm-up immediately preceding, but a higher HR response to SSE with no warm-up. Conclusion: The findings of this study suggest that a 10 minute delay following warm-up before SSE is too long to maintain the benefits of warm-up.

Effect of exercise on platelet activation during aspirin or clopidogrel intake in healthy men

Sudden strenuous exercise increases the risk of ischemic cardiac events in patients with coronary artery disease. The exact mechanism behind this observation is unknown, but platelet activation induced by exercise may be of importance. We hypothesized that brief strenuous exercise would activate platelets in healthy men, assessed by the Platelet Function Analyzer 100 and light transmittance aggregometry. Nearly all participants exhibited increased platelet reactivity after exercise measured by the Platelet Function Analyzer 100, whereas only minor changes were detected by light transmittance aggregometry. A significant increase in plasma von Willebrand Factor was also found in response to exercise. In conclusion, platelet activation occurs during exercise in healthy individuals. This activation is not prevented by use of aspirin or clopidogrel, and may partly be explained by an increase in plasma von Willebrand Factor.

Anomalous Origin of the Left Coronary Artery from the Pulmonary Artery (ALCAPA) in Four Calves

Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA), or Bland-White-Garland syndrome, is a rare congenital malformation described in children and adults. In this condition, the left coronary artery, which normally originates from the left coronary sinus in the aorta, instead originates from the pulmonary trunk, which results in retrograde flow of blood away from the myocardium into the lower-pressure pulmonary artery. Myocardial hypoxic-ischemic injury results in cardiac dysfunction, failure, and eventually in patient death if not surgically repaired. This report describes gross and microscopic findings in 4 beef calves with ALCAPA. All the calves had a history of being found dead with few or no premonitory signs, 2 shortly after sudden strenuous exercise. Gross necropsy lesions suggestive of heart failure included cardiomegaly with atrial and ventricular dilation and/or ventricular hypertrophy, and hepatomegaly. Dissection of each heart revealed the origin of the left coronary artery arising in the pulmonary trunk above the anterior cusp of the pulmonic valve. No degeneration; mineralization; and fiber loss, with replacement by fibrous connective tissue, predominantly in the left ventricular papillary muscle and the interventricular septum. Changes observed in the liver and lungs, including hepatomegaly, sinusoidal congestion, centrilobular fibrosis, and pulmonary congestion, edema, and intra-alveolar pigment-laden macrophages were consistent with heart failure.

Impaired cardiorespiratory response to brief sudden strenuous exercise in the postoperative tetralogy of fallot patients: a ten-second pedaling test.

No studies of cardiorespiratory response to brief, sudden, strenuous exercise in patients after tetralogy of Fallot (TOF) repair have been reported. We investigated the exercise capacity of TOF patients using a ten-second pedaling test designed to study cardiorespiratory responsiveness to brief, sudden, strenuous exercise. We assessed exercise capacity using a ten-second pedaling test (ten seconds maximal of voluntary cranking as fast as possible against an ergometer's inertial resistance), coupled with a conventional ramp-type progressive exercise test at a constant rate to the limit of tolerance, in eight male postoperative TOF patients and eight male control subjects. In the ten-second pedaling test, there were no significant differences in the integrated areas of heart rate (HR) and oxygen uptake () responses between the TOF patients and controls, but there were significantly longer decreasing phase time constants of HR and responses in the TOF patients than in the controls. In the conventional exercise test, the endurance time, peak-HR, and peak- did not differ between the groups. The TOF group, with a normal exercise capacity assessed by a conventional exercise test, had an impaired cardiorespiratory response to brief, sudden, strenuous exercise assessed by a ten-second pedaling test.

Cardiovascular response to sudden strenuous exercise: an exercise echocardiographic study.

We studied the response in left ventricular (LV) internal dimensions and posterior wall thickness during the performance of sudden strenuous exercise without warm-up (SSE) and sudden strenuous exercise with warm-up (SSEw) in 15 healthy, untrained college-aged males (26 +/- 5.0 yr). Measurements of left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic dimension (LVESD), stroke dimension (SD = LVEDD-LVESD), fractional shortening (FS = SD/EDD) and posterior wall thickness (PWT) were obtained from continuous 2-D targeted on M-mode echocardiography. Continuous EKG and blood pressure were obtained at rest and during the final 10 s of SSE (30 s of upright leg cycle ergometry of 400 W at 80 rpm). SSEw was preceded by warm-up exercise (6 min of graded leg cycle exercise of 2-min stages initial load 30 W, increasing in 30-W increments at 60 rpm, followed immediately by SSE). Our findings revealed that there were no significant differences in the LV internal dimensions (LVEDD, LVESD, FS, PWT), HR max, RPP max, ECG, and MAP max between SSE and SSEw. Sudden strenuous exercise without warm-up is not associated with a reduced LV function. The results of this study are contradictory to previous findings that have suggested that SSE is associated with transient global left ventricular (LV) dysfunction.

Cardiovascular Adaptations to Sudden Strenuous Exercise in Normal Subjects

To determine the hemodynamic adaptations during the earliest phase of exercise without warm-up, we performed first-pass radionuclide angiocardiography on 19 well-trained college athletes (mean age 19.7 ± 1.1 years, mean body surface area 1.96 ± 0.12 m^2) during sudden strenuous exercise. The subjects were studied at rest and at 20 and 45 s during exercise on a bicycle ergometer. Each attained the predetermined workload (2,700 kpm at 90 rpm) in 5-10 s and maintained that workload for the duration of the study. Maximal cardiac index occurred at 20 s in 5 subjects and at 45 s in 14 subjects. Measurements of change in heart rate (HR), systolic blood pressure, left ventricular ejection fraction (EF) and end-diastolic volume were more homogeneous when analyzed by the magnitude of cardiac output attained than by the time of measurement during exercise. The cardiac index (Cl) increased from 3.5 ±0.8 liters/min/m^2 at rest to 9.1 ± 2.3 liters/min/m^2 at the intermediate study level by an increase in HR (71 ± 12 to 156 ± 14 beats/min, p < 0.0001) and EF (0.59 ± 0.07 to 0.65 ± 0.07, p < 0.003). The transition to maximal Cl resulted from an increase in end-diastolic volume index (EDVI) (90 ± 22 to 107 ± 21 ml/m^2, p < 0.0007) through the Frank-Starling mechanism. Thus, during sudden strenuous exercise, Cl is raised to an intermediate level by an increase in HR and by enhancement of the contractile state of the myocardium leading to increased stroke volume index. Increase to maximal Cl occurs through an increase in EDVI and stroke volume index.

Cardiovascular response to sudden strenuous exercise.

Cardiac responses to sudden strenuous exercise were studied in seven dogs instrumented to measure cardiac output (Q), stroke volume (SV), left ventricular (LV) pressure, aortic pressure and circumflex coronary blood flow (CBF). The dogs were run on a treadmill at 12.9 km/h, 20% grade for 15s without prior warm-up. During the first 10s of the run, HR and Q increased rapidly. By 2s, myocardial O2 requirements, as estimated from either the tension time index (TTI) or calculated wall tension, had increased significantly above resting values. Simultaneously, mean CBF fell 13% and stroke CBF fell 49% below resting values at the onset of sudden exercise (2s) and was associated with 17% and 21% decreases in positive and negative LV dP/dt, a 9% decrease in (dP/dt)/P and an 11% decrease in SV. After the initial decrease at 2s, these variables then increased rapidly as the run continued except for stroke CBF which never reached resting levels. HR, Q, and LV dP/dt reached near maximal values for this level of exercise by 10s after the start of exercise. In contrast, mean CBF was still increasing when the run was terminated. These data show that sudden strenuous exercise results in a transient decrease in myocardial O2 delivery at a time when myocardial O2 requirements are rapidly increasing. This imbalance between myocardial O2 supply and demand is due to a transient decrease in coronary blood flow followed by a delay in metabolic regulation of CBF.

The Cardiac Response to Sudden Strenuous Exercise in the Post-Myocardial Infarction Patient Receiving Beta Blockers

The Cardiac Response to Sudden Strenuous Exercise in the Post-Myocardial Infarction Patient Receiving Beta Blockers

Effect of warm-up on left ventricular response to sudden strenuous exercise.

Sudden strenuous exercise (SSE) has been shown to produce ischemic electrocardiographic (ECG) responses, abnormalities of myocardial blood flow, and decreases in left ventricular ejection fraction. Prior exercise taken as warm-up has been shown to ameliorate the ECG and myocardial blood flow abnormalities induced by SSE. The purpose of this study was to determine whether warm-up would normalize the responses of the left ventricular ejection fraction to SSE. Twenty healthy male volunteers performed SSE (400-W bicycle exercise) either with (group A, n = 10) or without (group B, n = 10) warm-up. Ejection fraction was measured using first-pass radionuclide angiography under control conditions and during SSE. During SSE ejection fraction decreased from control values in both group A (70.5 +/- 6.3 to 64.8 +/- 8.2%) and group B (70.3 +/- 10.1 to 57.7 +/- 7.7%), although ejection fraction was significantly higher during SSE in group A. The results are consistent with the hypothesis that the abnormal responses to SSE are attributable to subendocardial ischemia secondary to a delay in autoregulation of myocardial blood flow. However, the decrease in ejection fraction during SSE even following warm-up suggests that the mechanism for the abnormal response to SSE is more complicated than previously hypothesized.

EFFECT OF WARM-UP ON LEFT VENTRICULAR RESPONSE TO SUDDEN STRENUOUS EXERCISE

Sudden strenuous exercise (SSE) has been shown to produce ischemic electrocardiographic (ECG) responses, abnormalities of myocardial blood flow, and decreases in left ventricular ejection fraction. Prior exercise taken as warm-up has been shown to ameliorate the ECG and myocardial blood flow abnormalities induced by SSE. The purpose of this study was to determine whether warm-up would normalize the responses of the left ventricular ejection fraction to SSE. Twenty healthy male volunteers performed SSE (400-W bicycle exercise) either with (group A, n = 10) or without (group B, n = 10) warm-up. Ejection fraction was measured using first-pass radionuclide angiography under control conditions and during SSE. During SSE ejection fraction decreased from control values in both group A (70.5 +/- 6.3 to 64.8 +/- 8.2%) and group B (70.3 +/- 10.1 to 57.7 +/- 7.7%), although ejection fraction was significantly higher during SSE in group A. The results are consistent with the hypothesis that the abnormal responses to SSE are attributable to subendocardial ischemia secondary to a delay in autoregulation of myocardial blood flow. However, the decrease in ejection fraction during SSE even following warm-up suggests that the mechanism for the abnormal response to SSE is more complicated than previously hypothesized.

Left ventricular function during sudden strenuous exercise.

Strenuous exercise without warm-up has been shown to produce ischemia-like electrocardiographic (ECG) abnormalities in 60-70% of healthy subjects. These abnormalities appeared to be related to the development of an unfavorable myocardial supply/demand balance and, in chronically instrumented dogs, to transient decreases in coronary blood flow. A mechanism involving subendocardial ischemia has been proposed to explain the response to sudden strenuous exercise (SSE). To determine whether the response to SSE included the development of changes in myocardial pump performance typical of ischemia, left ventricular (LV) function at rest, during graded exercise and during SSE was evaluated in nine young (26.6 +/- 3.4 years), well-trained male volunteers using first-pass radionuclide angiography. During graded exercise, the LV ejection fraction increased from 66.9 +/- 9.4% at rest to 73.0 +/- 7.1% during peak exercise, and the LV ejection rate increased from 3.36 +/- 0.67 sec-1 at rest to 6.58 +/- 1.10 sec-1 during peak exercise. Segmental wall motion was normal in all studies. During SSE, the LV ejection fraction decreased in very subject, from an average 72.2 +/- 8.6% at rst to 57.3 +/- 8.1% during exercise. The LV ejection rate remained relatively constant (3.98 +/- 0.92 sec-1 at rest vs 4.33 +/- 0.74 sec-1 during SSE). No segmental wall motion abnormalities were observed during SSE; however, LV wall motion appeared to be diffusely hypokinetic during SSE. In contrast to previous reports, few ECG abnormalities were observed during SSE. These results support the hypothesis that subendocardial ischemia is an important mechanism in the response to SSE. However, the lack of ECG changes and segmental wall motion abnormalities and the relatively high absolute value of the LV ejection fraction suggest that if subendocardial ischemia occurs during SSE, it is attributable to physiologic rather than pathologic mechanisms.

Ischemic response to sudden strenuous exercise in healthy men.

In ten healthy, asymptomatic men, intra-arterial pressure and electrocardiograms were recorded during various types of exercise. Potential subendocardial blood flow was estimated from a diastolic pressure time index (DPTI) and myocardial oxygen requirements estimated from the tension time index (TTI). The ratio DPTI/TTI provided an estimate of the supply/demand relationship With sudden vigorous exercise without warm-up, the DPTI/TTI was below 0.35 in three men who had ischemic electrocardiograms, below 0.44 in three men with minor ST abnormalities, and above 0.44 in four men with normal ST segments. With a prior warm-up exercise, sudden exercise caused no ischemic changes, but DPTI/TTI was below 0.44 in two subjects who had minor ST abnormalities. Maximum treadmill testing produced higher heart rates and TTI than did sudden exercise, but DPTI/TTI was above 0.44 in all cases and no ST abnormalities occurred. Abnormal electrocardiographic responses produced by sudden, vigorous exercise in normal men may represent subendocardial ischemia caused by a transient, unfavorable alteration in the subendocardial oxygen supply/demand relationship which is predictable from arterial pressure measurements.

Cardiovascular responses to sudden strenuous exercise--heart rate, blood pressure, and ECG.

Cardiovascular responses to sudden strenuous exercise--heart rate, blood pressure, and ECG.