Heart rate response to onset of exercise: evidence for enhanced cardiac sympathetic activity in animals susceptible to ventricular fibrillation

A large heart rate (HR) increase at the onset of exercise has been linked to an increased risk for adverse cardiovascular events, including cardiac death. However, the relationship between changes in cardiac autonomic regulation induced by exercise onset and the confirmed susceptibility to ventricular fibrillation (VF) has not been established. Therefore, a retrospective analysis of the HR response to exercise onset was made in mongrel dogs with healed myocardial infarctions that were either susceptible (S, n = 131) or resistant (R, n = 114) to VF (induced by a 2-min occlusion of the left circumflex artery during the last minute of exercise). The ECG was recorded, and time series analysis of HR variability (vagal activity index, the 0.24-1.04-Hz frequency component of R-R interval variability) was measured before and 30, 60, and 120 s after the onset of exercise (treadmill running). Exercise elicited significantly (ANOVA, P < 0.0001) greater increases in HR in susceptible dogs at all three times (e.g., at 60 s: R, 46.8 +/- 2.3 vs. S, 57.1 +/- 2.2 beats/min). However, the vagal activity index decreased to a similar extent in both groups of dogs (at 60 s: R, -2.8 +/- 0.1 vs. S, -3.0 +/- 0.2 ln ms2). Beta-adrenoceptor blockade (BB, propranolol 1.0 mg/kg iv) reduced the HR increase and eliminated the differences noted between the groups [at 60 s: R (n = 26), 40.4 +/- 3.2 vs. S (n = 31), 37.5 +/- 2.4 beats/min]. After BB, exercise once again elicited similar declines in vagal activity in both groups (at 60 s: R, -3.6 +/- 0.5 vs. S, -3.2 +/- 0.4 ln ms2). When considered together, these data suggest that at the onset of exercise HR increases to a greater extent in animals prone to VF compared with dogs resistant to this malignant arrhythmia due to an enhanced cardiac sympathetic activation in the susceptible dogs.     

Endurance exercise training attenuates cardiac beta2-adrenoceptor responsiveness and prevents ventricular fibrillation in animals susceptible to sudden death

Enhanced cardiac beta(2)-adrenoceptor (beta(2)-AR) responsiveness can increase susceptibility to ventricular fibrillation (VF). Exercise training can decrease cardiac sympathetic activity and could, thereby, reduce beta(2)-AR responsiveness and decrease the risk for VF. Therefore, dogs with healed myocardial infarctions were subjected to 2 min of coronary occlusion during the last minute of a submaximal exercise test; VF was observed in 20 susceptible, but not in 13 resistant, dogs. The dogs were then subjected to a 10-wk exercise-training program (n = 9 susceptible and 8 resistant) or an equivalent sedentary period (n = 11 susceptible and 5 resistant). Before training, the beta(2)-AR antagonist ICI-118551 (0.2 mg/kg) significantly reduced the peak contractile (by echocardiography) response to isoproterenol more in the susceptible than in the resistant dogs: -45.5 +/- 6.5 vs. -19.2 +/- 6.3%. After training, the susceptible and resistant dogs exhibited similar responses to the beta(2)-AR antagonist: -12.1 +/- 5.7 and -16.2 +/- 6.4%, respectively. In contrast, ICI-118551 provoked even greater reductions in the isoproterenol response in the sedentary susceptible dogs: -62.3 +/- 4.6%. The beta(2)-AR agonist zinterol (1 microM) elicited significantly smaller increases in isotonic shortening in ventricular myocytes from susceptible dogs after training (n = 8, +7.2 +/- 4.8%) than in those from sedentary dogs (n = 7, +42.8 +/- 5.8%), a response similar to that of the resistant dogs: +3.0 +/- 1.4% (n = 6) and +3.2 +/- 1.8% (n = 5) for trained and sedentary, respectively. After training, VF could no longer be induced in the susceptible dogs, whereas four sedentary susceptible dogs died during the 10-wk control period and VF could still be induced in the remaining seven animals. Thus exercise training can restore cardiac beta-AR balance (by reducing beta(2)-AR responsiveness) and could, thereby, prevent VF.     

Effect of training/detraining on submaximal exercise responses in humans

Human subjects participated in a training/detraining paradigm which consisted of 7 wk of intense endurance training followed by 3 wk of inactivity. In previously sedentary subjects, training produced a 23.9 +/- 7.2% increase in maximal aerobic power (V02max) (group S). Detraining did not affect group S V02max. In previously trained subjects (group T), the training/detraining paradigm did not affect V02max. In group S, training produced an increase in vastus lateralis muscle citrate synthase (CS) activities (nmol.mg protein-1. min-1) from 67.1 +/- 14.5 to 106.9 +/- 22.0. Detraining produced a decrease in CS activity to 80 +/- 14.6. In group T, pretraining CS activity (139.5 +/- 14.9) did not change in response to training. Detraining, however, produced a decrease in CS activity (121.5 +/- 7.8 to 66.8 +/- 5.9). Group S respiratory exchange ratios obtained during submaximal exercise at 60% V02max (R60) decreased in response to training (1.00 +/- 0.02 to 0.87 +/- 0.02) and increased (0.96 +/- 0.02) after detraining. Group T R60 (0.91 +/- 0.01) was not affected by training but increased (0.89 +/- 0.02 to 0.95 +/- 0.02) after detraining. R60 was correlated to changes in CS activity but was unrelated to changes in V02max. These data support the hypothesis that the mitochondrial content of working skeletal muscle is an important determinant of substrate utilization during submaximal exercise.     

Effect of dietary omega-3 fatty acids on the heart rate and the heart rate variability responses to myocardial ischemia or submaximal exercise

The consumption of omega-3 polyunsaturated fatty acids (n-3 PUFAs) has been reported to decrease resting heart rate (HR) and increase heart rate variability (HRV). However, the effects of n-3 PUFAs on these variables in response to a physiological stress (e.g., exercise or acute myocardial ischemia), particularly in postmyocardial infarction (MI) patients, are unknown. Therefore, HR and HRV (high frequency and total R-R interval variability) were evaluated at rest, during submaximal exercise, and during a 2-min coronary artery occlusion at rest and before and 3 mo after n-3 PUFA treatment in dogs with healed MI (n = 59). The dogs were randomly assigned to either placebo (1 g/day corn oil, n = 19) or n-3 PUFA supplement (docosahexaenoic acid + eicosapentaenoic acid ethyl esters; 1 g/day, n = 6; 2 g/day, n = 12; or 4 g/day, n = 22) groups. The treatment elicited significant (P < 0.01) dose-dependent increases in right atrial n-3 PUFA levels but dose-independent reductions in resting HR and increases in resting HRV. In contrast, n-3 PUFAs did not attenuate the large changes in HR or HRV induced by either the coronary occlusion or submaximal exercise. These data demonstrate that dietary n-3 PUFA decreased resting (i.e., preexercise or preocclusion) HR and increased resting HRV but did not alter the cardiac response to physiologic challenges.     

Endurance training of older men: responses to submaximal exercise.

The purpose of this study was to quantify the exercise response of older subjects on a time-to-fatigue (TTF) submaximal performance test before and after a training program. Eight older men (67.4 +/- 4.8 yr) performed two maximal treadmill tests to determine maximum oxygen uptake (VO2max) and ventilation threshold (TVE) and a constant-load submaximal exercise treadmill test that required an oxygen uptake (VO2) between TVE and VO2max. The submaximal test, performed at the same absolute work rate before and after the training program, was performed to volitional fatigue to measure endurance time. The men trained under supervision at an individualized pace representing approximately 70% of VO2max (80% maximum heart rate) for 1 h, four times per week for 9 wk. Significant increases were demonstrated for VO2max (ml.kg-1.min-1; 10.6%); maximal ventilation (VE, l/min; 11.6%), and TVE (l/min; 9.8%). Weight decreased 2.1%. Performance time on the TTF test increased by 180% (7.3 +/- 3.0 to 20.4 +/- 13.5 min). The similar end points for VO2, VE, and heart rate during the TTF and maximal treadmill tests established that the TTF test was stopped because of physiological limitations. The increase in performance time among the subjects was significantly correlated with improvements in VO2max and TVE, with the submaximal work rate representing a VO2 above TVE by 88% of the difference between TVE and VO2max pretraining and 73% of this difference on posttraining values.     

Plasma norepinephrine and heart rate dynamics during recovery from submaximal exercise in man

The time course of heart rate (HR) and venous blood norepinephrine concentration [NE], as an expression of the sympathetic nervous activity (SNA), was studied in six sedentary young men during recovery from three periods of cycle ergometer exercise at 21% +/- 2.8%, 43% +/- 2.1% and 65% +/- 2.3% of VO2max respectively (mean +/- SE). The HR decreased mono-exponentially with tau values of 13.6 +/- 1.6 s, 32.7 +/- 5.6 s and 55.8 +/- 8.1 s respectively in the three periods of exercise. At the low exercise level no change in [NE] was found. At medium and high exercise intensity: (a) [NE] increased significantly at the 5th min of exercise (delta [NE] = 207.7 +/- 22.5 pg.ml-1 and 521.3 +/- 58.3 pg.ml-1 respectively); (b) after a time lag of 1 min [NE] decreased exponentially (tau = 87 s and 101 s respectively); (c) in the 1st min HR decreased about 35 beats.min-1; (d) from the 2nd to 5th min of recovery HR and [NE] were linearly related (100 pg.ml-1 delta [NE] congruent to 5 beats.min-1). In the 1st min of recovery, independent of the exercise intensity, the adjustment of HR appears to have been due mainly to the prompt restoration of vagal tone. The further decrease in HR toward the resting value could then be attributed to the return of SNA to the pre-exercise level.     

Variation in heart rate during submaximal exercise: implications for monitoring training

A change in heart rate at a controlled submaximal exercise intensity is used as a marker of training status. However, the standard error of measurement has not been studied systematically, and therefore a change in heart rate, which can be considered relevant, has not been determined. Forty-four subjects (26.5 +/- 5.4 years; mean +/- standard deviation) participated in a submaximal running test at the same time of day for 5 consecutive days. Heart rates were determined during each of the 4 exercise intensities (2 minutes each) of increasing intensity and during the 1-minute recovery period after each stage. The repeatability of the heart rate on a day-to-day basis during the stages and recovery periods were high (intraclass correlation coefficient: 95% confidence interval R = 0.94- 0.99). The lowest variation in heart rate occurred in the fourth stage ( approximately 90% maximum heart rate) with heart rate varying 5 +/- 2 b.min(-1) (95% confidence interval for coefficient of variation = 1.1-1.4%). In conclusion, the standard error of measurement of submaximal heart rate is 1.1-1.4%. This magnitude of measurement error needs to be considered when heart rate is used as a marker of training status.     

Heritability of submaximal exercise heart rate response to exercise training is accounted for by nine SNPs

Endurance training-induced changes in hemodynamic traits are heritable. However, few genes associated with heart rate training responses have been identified. The purpose of our study was to perform a genome-wide association study to uncover DNA sequence variants associated with submaximal exercise heart rate training responses in the HERITAGE Family Study. Heart rate was measured during steady-state exercise at 50 W (HR50) on 2 separate days before and after a 20-wk endurance training program in 483 white subjects from 99 families. Illumina HumanCNV370-Quad v3.0 BeadChips were genotyped using the Illumina BeadStation 500GX platform. After quality control procedures, 320,000 single-nucleotide polymorphisms (SNPs) were available for the genome-wide association study analyses, which were performed using the MERLIN software package (single-SNP analyses and conditional heritability tests) and standard regression models (multivariate analyses). The strongest associations for HR50 training response adjusted for age, sex, body mass index, and baseline HR50 were detected with SNPs at the YWHAQ locus on chromosome 2p25 (P = 8.1 × 10(-7)), the RBPMS locus on chromosome 8p12 (P = 3.8 × 10(-6)), and the CREB1 locus on chromosome 2q34 (P = 1.6 × 10(-5)). In addition, 37 other SNPs showed P values <9.9 × 10(-5). After removal of redundant SNPs, the 10 most significant SNPs explained 35.9% of the ΔHR50 variance in a multivariate regression model. Conditional heritability tests showed that nine of these SNPs (all intragenic) accounted for 100% of the ΔHR50 heritability. Our results indicate that SNPs in nine genes related to cardiomyocyte and neuronal functions, as well as cardiac memory formation, fully account for the heritability of the submaximal heart rate training response.     

Influence of training on sweating responses during submaximal exercise in horses.

Sweating responses were examined in five horses during a standardized exercise test (SET) in hot conditions (32-34 degrees C, 45-55% relative humidity) during 8 wk of exercise training (5 days/wk) in moderate conditions (19-21 degrees C, 45-55% relative humidity). SETs consisting of 7 km at 50% maximal O(2) consumption, determined 1 wk before training day (TD) 0, were completed on a treadmill set at a 6 degrees incline on TD0, 14, 28, 42, and 56. Mean maximal O(2) consumption, measured 2 days before each SET, increased 19% [TD0 to 42: 135 +/- 5 (SE) to 161 +/- 4 ml. kg(-1). min(-1)]. Peak sweating rate (SR) during exercise increased on TD14, 28, 42, and 56 compared with TD0, whereas SRs and sweat losses in recovery decreased by TD28. By TD56, end-exercise rectal and pulmonary artery temperature decreased by 0.9 +/- 0.1 and 1.2 +/- 0.1 degrees C, respectively, and mean change in body mass during the SET decreased by 23% (TD0: 10.1 +/- 0.9; TD56: 7.7 +/- 0.3 kg). Sweat Na(+) concentration during exercise decreased, whereas sweat K(+) concentration increased, and values for Cl(-) concentration in sweat were unchanged. Moderate-intensity training in cool conditions resulted in a 1.6-fold increase in sweating sensitivity evident by 4 wk and a 0.7 +/- 0.1 degrees C decrease in sweating threshold after 8 wk during exercise in hot, dry conditions. Altered sweating responses contributed to improved heat dissipation during exercise and a lower end-exercise core temperature. Despite higher SRs for a given core temperature during exercise, decreases in recovery SRs result in an overall reduction in sweat fluid losses but no change in total sweat ion losses after training.     

Cardiac vagal modulation of heart rate during prolonged submaximal exercise in animals with healed myocardial infarctions: effects of training

The present study investigated the effects of long-duration exercise on heart rate variability [as a marker of cardiac vagal tone (VT)]. Heart rate variability (time series analysis) was measured in mongrel dogs (n = 24) with healed myocardial infarctions during 1 h of submaximal exercise (treadmill running at 6.4 km/h at 10% grade). Long-duration exercise provoked a significant (ANOVA, all P < 0.01, means +/- SD) increase in heart rate (1st min, 165.3 +/- 15.6 vs. last min, 197.5 +/- 21.5 beats/min) and significant reductions in high frequency (0.24 to 1.04 Hz) power (VT: 1st min, 3.7 +/- 1.5 vs. last min, 1.0 +/- 0.9 ln ms(2)), R-R interval range (1st min, 107.9 +/- 38.3 vs. last min, 28.8 +/- 13.2 ms), and R-R interval SD (1st min, 24.3 +/- 7.7 vs. last min 6.3 +/- 1.7 ms). Because endurance exercise training can increase cardiac vagal regulation, the studies were repeated after either a 10-wk exercise training (n = 9) or a 10-wk sedentary period (n = 7). After training was completed, long-duration exercise elicited smaller increases in heart rate (pretraining: 1st min, 156.0 +/- 13.8 vs. last min, 189.6 +/- 21.9 beats/min; and posttraining: 1st min, 149.8 +/- 14.6 vs. last min, 172.7 +/- 8.8 beats/min) and smaller reductions in heart rate variability (e.g., VT, pretraining: 1st min, 4.2 +/- 1.7 vs. last min, 0.9 +/- 1.1 ln ms(2); and posttraining: 1st min, 4.8 +/- 1.1 vs. last min, 2.0 +/- 0.6 ln ms(2)). The response to long-duration exercise did not change in the sedentary animals. Thus the heart rate increase that accompanies long-duration exercise results, at least in part, from reductions in cardiac vagal regulation. Furthermore, exercise training attenuated these exercise-induced reductions in heart rate variability, suggesting maintenance of a higher cardiac vagal activity during exercise in the trained state.     

Early effects of short-term endurance training on hormonal responses to graded exercise.

Twelve male, sedentary volunteers (22.0 +/-) were submitted to three weeks of a bicycle ergometer training, consisting of 45 min exercise (at 70% VO2max), 4 times in the first week and 3 times in the next 2 weeks. They performed four incremental exercise tests with the power output increased by 50 W every 3 min until volitional exhaustion: two before training (C1 and C2), and after one (T1) and three (T3) weeks of training. Before and after each load the plasma noradrenaline (NA), adrenaline (A) and blood lactate (LA) concentrations were determined in venous blood samples as well as plasma growth hormone (HGH) and cortisol concentrations before and at the end of exercise. A decrease in NA concentration was found already after 1 week of training at power output of 100 W (p<0.01) and 200 W (p<0.05). Similar decline was maintained after 3 weeks of training. No significant training-induced differences in plasma A concentration were found, however, the thresholds for both catecholamines were significantly shifted towards higher values after 3 weeks of training. One week of training caused a decrease in the pre-exercise (p<0.01), as well as post-exercise (p<0.05) plasma cortisol and HGH concentrations. It was concluded that endurance training induced a decrease in HGH, cortisol and NA concentration already after one week of training. A decline of pre-exercise plasma HGH and cortisol levels with time of experiment may, in part, indicate familiarization to exercise protocol.     

Exercise training normalizes beta-adrenoceptor expression in dogs susceptible to ventricular fibrillation

Previous studies demonstrated an enhanced beta(2)-adrenoceptor (AR) responsiveness in animals susceptible to ventricular fibrillation (VF) that was eliminated by exercise training. The present study investigated the effects of endurance exercise training on beta(1)-AR and beta(2)-AR expression in dogs susceptible to VF. Myocardial ischemia was induced by a 2-min occlusion of the left circumflex artery during the last minute of exercise in dogs with healed infarctions: 20 had VF [susceptible (S)] and 13 did not [resistant (R)]. These dogs were randomly assigned to either 10-wk exercise training [treadmill running; n = 9 (S) or 8 (R)] or an equivalent sedentary period [n = 11 (S) or 5 (R)]. Left ventricular tissue beta-AR protein and mRNA were quantified by Western blot analysis and RT-PCR, respectively. Because beta(2)-ARs are located in caveolae, caveolin-3 was also quantified. beta(1)-AR gene expression decreased ( approximately 5-fold), beta(2)-AR gene expression was not changed, and the ratio of beta(2)-AR to beta(1)-AR gene expression was significantly increased in susceptible compared with resistant dogs. beta(1)-AR protein decreased ( approximately 50%) and beta(2)-AR protein increased (400%) in noncaveolar fractions of the cell membrane in susceptible dogs. Exercise training returned beta(1)-AR gene expression to levels seen in resistant animals but did not alter beta(2)-AR protein levels in susceptible dogs. These data suggest that beta(1)-AR gene expression was decreased in susceptible dogs compared with resistant dogs and, further, that exercise training improves beta(1)-AR gene expression, thereby restoring a more normal beta-AR balance.     

Effects of residential exercise training on heart rate recovery in coronary artery patients

The aims of the present study are twofold: 1) to investigate whether heart rate recovery (HRR) after a cycle ergometry test is affected by exercise training and 2) to test the ability of HRR to replicate the baroreflex sensitivity (BRS) changes that occur in response to an exercise training program in coronary artery patients. We randomized 82 coronary artery patients undergoing a residential cardiac rehabilitation program to an exercise training group (TR; n = 43) and an untrained group (UTR; n = 39). All of the patients underwent an exercise test before and after the rehabilitation program. HRR was recorded at the end of the 1st and 2nd min after exercise. BRS was determined at rest before and after treatment. HRR after the 2nd min was significantly improved in TR patients (-21.4 +/- 0.9 beats/min) compared with UTR patients (-17.8 +/- 1.2 beats/min) at the end of the training program. Improvement in HRR paralleled that in BRS in TR patients (from 3.2 +/- 0.3 to 5.3 +/- 0.8 ms/mmHg; P < 0.001), whereas no significant change was evident in UTR patients (from 3.5 +/- 0 to 4.0 +/- 0.4 ms/mmHg; P = 0.230). Our data show that HRR in the 2nd min after the cessation of a cycle ergometer exercise test increased in coronary artery patients after an exercise training period. This result confirms the positive effect induced by exercise training on HRR and extends the conclusions of previous studies to different modalities of exercise (i.e., cycle ergometer). HRR might provide an additional simple marker of the effectiveness of physical training programs in cardiac patients.     

Effects of 7 wk of endurance training on human skeletal muscle metabolism during submaximal exercise.

This is the first study to examine the effects of endurance training on the activation state of glycogen phosphorylase (Phos) and pyruvate dehydrogenase (PDH) in human skeletal muscle during exercise. We hypothesized that 7 wk of endurance training (Tr) would result in a posttransformationally regulated decrease in flux through Phos and an attenuated activation of PDH during exercise due to alterations in key allosteric modulators of these important enzymes. Eight healthy men (22 +/- 1 yr) cycled to exhaustion at the same absolute workload (206 +/- 5 W; approximately 80% of initial maximal oxygen uptake) before and after Tr. Muscle biopsies (vastus lateralis) were obtained at rest and after 5 and 15 min of exercise. Fifteen minutes of exercise post-Tr resulted in an attenuated activation of PDH (pre-Tr: 3.75 +/- 0.48 vs. post-Tr: 2.65 +/- 0.38 mmol.min(-1).kg wet wt(-1)), possibly due in part to lower pyruvate content (pre-Tr: 0.94 +/- 0.14 vs. post-Tr: 0.46 +/- 0.03 mmol/kg dry wt). The decreased pyruvate availability during exercise post-Tr may be due to a decreased muscle glycogenolytic rate (pre-Tr: 13.22 +/- 1.01 vs. post-Tr: 7.36 +/- 1.26 mmol.min(-1).kg dry wt(-1)). Decreased glycogenolysis was likely mediated, in part, by posttransformational regulation of Phos, as evidenced by smaller net increases in calculated muscle free ADP (pre-Tr: 111 +/- 16 vs. post-Tr: 84 +/- 10 micromol/kg dry wt) and P(i) (pre-Tr: 57.1 +/- 7.9 vs. post-Tr: 28.6 +/- 5.6 mmol/kg dry wt). We have demonstrated for the first time that several signals act to coordinately regulate Phos and PDH, and thus carbohydrate metabolism, in human skeletal muscle after 7 wk of endurance training.     

Effect of energy drink dose on exercise capacity,heart rate recovery and heart rate variability after high-intensity exercise

[Purpose]

The purpose of this research was to investigate the effects of exercise capacity, heart rate recovery and heart rate variability after high-intensity exercise on caffeine concentration of energy drink.

[Methods]

The volunteers for this study were 15 male university student. 15 subjects were taken basic physical examinations such as height, weight and BMI before the experiment. Primary tests were examined of VO₂max per weight of each subjects by graded exercise test using Bruce protocol. Each of five subject was divided 3 groups (CON, ECGⅠ, ECGⅡ) by matched method based on weight and VO₂max per weight what gained of primary test for minimize the differences of exercise capacity and ingestion of each groups. For the secondary tests, the groups of subjects were taken their materials before and after exercise as a blind test. After the ingestion, subjects were experimented on exercise test of VO₂max 80% by treadmill until the all-out. Heart rate was measured by 1minute interval, and respiratory variables were analyzed VO2, VE, VT, RR and so on by automatic respiratory analyzer. And exercise exhaustion time was determined by stopwatch. Moreover, HRV was measured after exercise and recovery 3 min.

[Results]

Among the intake groups, ECGⅡ was showed the longest of exercise exhaustion time more than CON group (p = .05). Result of heart rate during exercise according to intake groups, there was significant differences of each time (p < .001), however, not significant differences of each groups and group verse time (p > .05). Result of RPE during exercise according to intake groups, there was significant differences of each time (p < .001), however, not significant differences of each groups and group verse time (p > .05).

[Conclusion]

In conclusion, EDGⅡ showed the significant increase of exercise exhaustion time more than CON group (p=.05) and not significant differences in HR, RPE, RER, HRV, HRR, blood pressure (p > .05). Therefore, 2.5 mg/kg^-1 ingestion of energy drink might be positive effect to increase exercise performance capacity without side-effect in cardiovascular disease.     

Effects of detraining on responses to submaximal exercise

Seven endurance-trained subjects were studied 12, 21, 56, and 84 days after cessation of training. Heart rate, ventilation, respiratory exchange ratio, and blood lactate concentration during submaximal exercise of the same absolute intensity increased (P less than 0.05) progressively during the first 56 days of detraining, after which a stabilization occurred. These changes paralleled a 40% decline (P less than 0.001) in mitochondrial enzyme activity levels and a 21% increase in total lactate dehydrogenase (LDH) activity (P less than 0.05) in trained skeletal muscle. After 84 days of detraining, the experimental subjects' muscle mitochondrial enzyme levels were still 50% above, and LDH activity was 22% below, sedentary control levels. The blood lactate threshold of the detrained subjects occurred at higher absolute and relative (i.e., 75 +/- 2% vs. 62 +/- 3% of maximal O2 uptake) exercise intensities in the subjects after 84 days of detraining than in untrained controls (P less than 0.05). Thus it appears that a portion of the adaptation to prolonged and intense endurance training that is responsible for the higher lactate threshold in the trained state persists for a long time (greater than 85 days) after training is stopped.     

Heart rate recovery and heart rate complexity following resistance exercise training and detraining in young men

The purpose of this study was to examine heart rate recovery (HRR) and linear/nonlinear heart rate variability (HRV) before and after resistance training. Fourteen young men (25.0 +/- 1.1 yr of age) completed a crossover design consisting of a 4-wk time-control period, 6 wk of resistance training (3 days/wk), and 4 wk of detraining. Linear HRV was spectrally decomposed using an autoregressive approach. Nonlinear dynamics of heart rate complexity included sample entropy (SampEn) and Lempel-Ziv entropy (LZEn). HRR was calculated from a graded maximal exercise test as maximal heart rate attained during the test minus heart rate at 1 min after exercise (HRR). There was no change in SampEn, LZEn, or HRR after the time-control portion of the study (P > 0.05). SampEn (P < 0.05), LZEn (P < 0.05), and HRR (P < 0.05) increased after resistance training and returned to pretraining values after detraining. There was no change in spectral measures of HRV at any time point (P > 0.05). These findings suggest that resistance exercise training increases heart rate complexity and HRR after exercise but has no effect on spectral measures of HRV in young healthy men. These autonomic changes regress shortly after cessation of training.     

The impact of endurance exercise training on left ventricular systolic mechanics

Although exercise training-induced changes in left ventricular (LV) structure are well characterized, adaptive functional changes are incompletely understood. Detailed echocardiographic assessment of LV systolic function was performed on 20 competitive rowers (10 males and 10 females) before and after endurance exercise training (EET; 90 days, 10.7 +/- 1.1 h/wk). Structural changes included LV dilation (end-diastolic volume = 128 +/- 25 vs. 144 +/- 28 ml, P < 0.001), right ventricular (RV) dilation (end-diastolic area = 2,850 +/- 550 vs. 3,260 +/- 530 mm2, P < 0.001), and LV hypertrophy (mass = 227 +/- 51 vs. 256 +/- 56 g, P < 0.001). Although LV ejection fraction was unchanged (62 +/- 3% vs. 60 +/- 3%, P = not significant), all direct measures of LV systolic function were altered. Peak systolic tissue velocities increased significantly (basal lateral S'Delta = 0.9 +/- 0.6 cm/s, P = 0.004; and basal septal S'Delta = 0.8 +/- 0.4 cm/s, P = 0.008). Radial strain increased similarly in all segments, whereas longitudinal strain increased with a base-to-apex gradient. In contrast, circumferential strain (CS) increased in the LV free wall but decreased in regions adjacent to the RV. Reductions in septal CS correlated strongly with changes in RV structure (DeltaRV end-diastolic area vs. DeltaLV septal CS; r2 = 0.898, P < 0.001) and function (Deltapeak RV systolic velocity vs. DeltaLV septal CS, r2 = 0.697, P < 0.001). EET leads to significant changes in LV systolic function with regional heterogeneity that may be secondary to concomitant RV adaptation. These changes are not detected by conventional measurements such as ejection fraction.