Peter A. Farrell

Enkephalins, catecholamines, and psychological mood alterations: effects of prolonged exercise

Seven healthy trained men were studied to determine if running at various relative intensities [percent maximal oxygen consumption (VO2max)] alters peripheral venous levels of leucine enkephalin-like material. Enkephalins were measured using a radio-receptor assay (Leu-Enk RRA). Subjects ran for 80 min at 40 and 60% VO2max and for 40 min at 80% VO2max. Each session was separated by at least 1 wk. Heart rate, blood pressure, lactic acid, and rectal temperature responses increased in an intensity-dependent manner. Epinephrine increased from resting values of 38.2 +/- 6.8 pg X ml-1, mean +/- SE to 75.0 +/- 13.3 pg X ml-1 during the 40% VO2max run, from 60.2 +/- 15 to 186 +/- 45 pg X ml-1 during the 60% run, and from 33.4 +/- 7.6 to 311 +/- 52 pg X ml-1 at the 40th min of the highest workload (80% VO2max). These increases were significant (P less than 0.05). Plasma Leu-Enk RRA was between 3.8 and 6.2 pmol X ml-1 prior to each run and did not change significantly as a result of exercise. Levels of Leu-Enk RRA also did not change during 30 min of supine recovery. Perception of effort increased (P less than 0.05) with increases in exercise intensity, and effort sense was unrelated to plasma Leu-Enk RRA. Psychological tension decreased significantly (P less than 0.05) following exercise at 60 and 80% of VO2max, but the decrease following the 40% run was not significant (P greater than 0.05). Reduced tension following exercise was not related to Leu-Enk RRA.(ABSTRACT TRUNCATED AT 250 WORDS)

The time course of alterations in plasma lipid and lipoprotein concentrations during eight weeks of endurance training.

Sixteen subjects (male = 7, female = 9) participated in 8 weeks of endurance training (70% VOmax, 30 min/day, 3--4 days/wk). Plasma lipid and lipoprotein concentrations in venous blood were assessed prior to and at 2-week intervals during the 8 weeks of training. VO2max was determined prior to training and at 4-week intervals. Body composition was assessed pre- and post-training. Results indicate that after an insignificant decline at 2 weeks (53.8 leads to 51.1 mg/dl), plasma high density lipoproteins (HDL) increased significantly (P < 0.05) at 8 weeks of training (51.1 leads to 57.4 mg/dl). This increase was linear after 2 weeks (r = 0.98) with a slope of +1 mg/dl/wk. This pattern of change was similar in males and females. VO2max (42.2 leads to 43.8 leads to 45.9 ml/kg x min) and time to exhaustion on the treadmill (6.9 leads to 8.0 leads to 9.1 min) increased significantly (P < 0.05) during training. Relative fat was not related to any lipid or lipoprotein group. Total cholesterol showed wide variations between sampling periods but was not significantly changed during the training period. Plasma triglycerides decreased significantly from 4 to 8 weeks of training, a period when HDLs were increasing. Over the last 4 weeks of training, the relationship between HDLs and triglycerides was significant, r = --0.65 (P < 0.05). These results suggest that alterations in HDLs lag behind changes in total cardiovascular fitness and increase simultaneously with a decline in plasma triglycerides after 4 weeks of endurance training.

A comparison of plasma cholesterol, triglycerides. and high density lipoprotein-cholesterol in speed skaters, weightlifters and non-athletes

SummaryVenous plasma cholesterol, triglycerides and high-density lipoprotein cholesterol (HDL-C) were measured after a 12–16 h overnight fast in three groups of men with different physical training histories. The groups consisted of 11 untrained men (aged 19–25 years), 11 well-trained weightlifters (20–32 years), who had not trained aerobically for at least 6 months, and 11 candidates for an Olympic speed skating team (17–27 years), whose training was both endurance (aerobic) and anaerobic. Mean maximal oxygen uptakes for the groups were 47.7, 45.7, and 62.3 ml·kg−1·min−1 respectively. Groups were similar with respect to diet, smoking and alcohol consumption, but the nonathletes were fatter, the weightlifters older and the speed skaters lighter, than the others. There were no significant differences in total cholesterol or triglycerides between the groups. Mean HDL-C was similar in the non-athletes and weightlifters [about 47±7 (SD) mg·dl−1], but was significantly higher (53.7±10.2 mg·dl−1, p<0.05) in the speed skaters. It was not correlated significantly with maximal oxygen uptake or relative fat in any group or when all data were combined. The total cholesterol/HDL-C ratio was significantly higher in the weightlifters. The HDL-C values are compared with previously reported values for non-athletes and athletes, and it is concluded that extensive weight-training, in contrast to endurance training, does not increase venous plasma HDL-C. Further work is required to elucidate the biochemical basis of these observations.

Exercise and endorphins—male responses

The discovery of the endogenous opiates in the mid-1970s has led to a tremendous scientific effort attempting to determine the physiological role of these peptides. An increase in the peripheral plasma levels of beta-endorphin in humans after exercise has been noted by all investigators to date. This indication that the endogenous opiate system is activated during exercise should stimulate investigators to use exercise and training as models to aid in the understanding of these peptides. Unlike most other endocrines, plasma levels of beta-endorphin do not increase proportionally to work intensity. This conclusion is based on only one study and requires corroboration. All human studies to date have used radioimmunoassays, with one exception, and interestingly that study showed no consistent change in plasma levels of leucine enkephalin-like radioreceptor assayable ligands. In males, essentially no information is available concerning the effects of training on either acute or chronic responses to exercise. Studies using opiate antagonists (receptor type-specific) in human and animal models should prove useful in establishing or disproving roles for these peptides in appetite, pain perception, temperature regulation, metabolism, ventilation, and blood pressure control during exercise.

Body composition of Olympic speed skating candidates.

Abstract The purpose of this investigation was to quantify the body composition of speed skaters who were candidates for the 1980 United States Olympic Team. Subjects were 19 males between 16 and 27 years of age. Most subjects had just completed three months of intensive dry-land training. Seven skinfold fat, 11 circumference, and seven diameter sites were measured. Body density was determined by underwater weighing. Study of the speed skaters (mean ± standard deviation) gave the following results: height, 176 ± 8 cm; body weight, 69.6 ± 7.0 kg; body density, 1.081 ± 0.006 g/ml; and relative fat, 7.6 ± 2.6%. The eight speed skaters who were selected for the Olympic Team were significantly older, taller, and heavier in total body weight and fat free weight (FFW) than the non-Olympians. Thus, years of training and greater FFW may help differentiate international caliber male speed skaters. Data on Olympic speed skating candidates from 1968 showed them to be of similar age (20.1 yr) and height (176 cm), but ...

Time course of lung volume changes during prolonged treadmill exercise

It has been known since the 1920s that runners completing marathon races have reduced forced vital capacity (FVC) values. To investigate the time course of these lung volume alterations, we measured FVC and residual volume (RV) in 11 runners before, after, and at 30-min intervals during a 2.5-h treadmill run at just under their marathon pace (70% VO2max). Mean distance run was 21.5 +/- 1.5 (SD) miles in the 2.5-h period. During the first 60 min, both RV and total lung capacity (TLC) decreased by 110 ml, however, this change was not significant (P greater than 0.05). A high correlation (r = 0.93) was observed between delta RV and delta TLC during the first 5 min, while FVC remained unchanged. From 60-90 min, all lung volumes remained constant. From 90-150 min, lung volumes changed in a direction similar to that observed after a marathon, i.e., FVC decreased significantly (5.51 to 5.37 liter between 90 and 150 min, P less than 0.05), TLC remained unchanged (7.41 vs 7.42 liter, P greater than 0.05), and RV showed a nonsignificant increase from 1.90 to 2.05 liter (P greater than 0.05). The data are consistent with multiple mechanisms playing a role in pulmonary function changes during prolonged exercise. The smaller mean decrease in FVC observed in this study, as compared to that found during a marathon, suggested that the marathon imposes a greater demand on the lungs than did treadmill exercise of the duration and relative intensity used in this study.

Effect of exercise training on the onset of type I diabetes in the BB/Wor rat.

The effects of regular exercise training on the onset and/or severity of hyperglycemia were studied in female diabetes-prone Biobreeding/Worcester (DP BB/Wor) rats. At 38-39 d of age, animals were weight-matched and randomly assigned to exercise-trained (T) and untrained (Unt) groups. The T rats exercised on a rodent treadmill at a moderate workload, 5 successive days with the 6th day being one of rest. Training lasted 5-11 wk until rats became moribund. Red gastrocnemius muscle citrate synthase activity was significantly higher in T (54.2 +/- 4.7 mumol.g-1.min-1) compared with Unt (42.9 +/- 5.1). No significant difference was found between the T and Unt groups in the following: age at onset of hyperglycemia (T = 82.9 +/- 8.7 d; Unt = 82.0 +/- 13.5 d, mean +/- SD), ultimate level of hyperglycemia, age of death (T = 89.9 +/- 9.2 d; Unt = 89.4 +/- 13.9 d), number of days between onset of hyperglycemia and death, or body weights at the onset of hyperglycemia. No significant difference was found between groups in pancreatic insulin concentration (microgram.g-1 of protein), T = 0.22 +/- 0.04; Unt = 0.20 +/- 0.34. These data suggest that a program of regular exercise training may not delay the onset and/or reduce the severity of hyperglycemia in the DP BB/Wor rat. Regular exercise training had no beneficial or detrimental effect on pancreatic beta-cell destruction.

Decreased insulin response to sustained hyperglycemia in exercise-trained rats

Male Wistar rats were studied to determine if exercise training reduces the insulin response to sustained hyperglycemia. Training (TN) for 8 wk on a treadmill resulted in significantly (P less than 0.05) increased time to exhaustion in TN compared to control animals (CN). Hyperglycemic glucose clamps at 11 mM for 90 min resulted in elevations of arterial plasma insulin to 23.6 +/- 4.3 ng.ml-1 (mean +/- SE, N = 7) in CN and 11.8 +/- 1.1 ng.ml-1 (N = 7) in TN (P less than 0.05). No significant difference between groups existed for the level of imposed hyperglycemia. Glucose infusion rates required to maintain the sustained hyperglycemia were 62.7 +/- 3.2 mg.kg-1 min-1 in CN and 68.5 +/- 3.0 mg.kg-1.min-1 in TN (P greater than 0.05) at the end of the glucose clamp. These data show that exercise training reduces the insulin response to sustained steady state hyperglycemia.

Exercise Stress and Endogenous Opiates

The use of exercise to reveal physiological responses and adaptations has a long history. Exercise can be quantified and repeated exertion markedly alters body functions. Well established exercise procedures such as the use of an individual’s aerobic capacity have allowed exercise stress to be used as an experimental model to investigate the endogenous opiate system. A vast literature had accumulated prior to 1975 concerning the physiological effects of morphine. When the endogenous opiates were discovered’, researchers already had insights into probable functions of the endogenous opiates. Therefore, it is not surprising that many possible roles for endorphins/enkephalins have been studied using the exercise model.

Plasma beta endorphin immunoreactivity: Effects of sustained hyperglycemia with and without prior exercise

Abstract Seven healthy untrained men were studied to determine if sustained hyperglycemia is a stimulus to enhanced plasma levels of beta endorphin (β-EP) and if so whether prior exercise affects that enhancement. After an overnight fast hyperglycemia glucose clamps were performed on 3 separate days: after prior rest, 2 h after exercise, and 48 h after exercise. Subjects exercised on a bicycle ergometer for 1 h at 150 W (64% VO 2 max). Plasma glucose concentration was elevated in 4 continuous sequential stages to 7, 11, 20 and 35 mM with each stage lasting 90 min. Plasma glucose concentrations did not differ for each subject across the three clamps. β-EP immunoreactivity was measured in arterialized venous blood samples using a specific and sensitive radioimmunoassay. Resting β-EP at basal glucose concentrations was 3.8±0.7 fmol·ml −1 (mean ± se) and prior exercise either 2h (3.2± 0.5 fmol·ml −1 ) or 48 h (4.3± 0.7 fmol·ml −1 ) before a clamp study did not effect these levels, (p > 0.05). At no time during the 3 hyperglycemic clamps did plasma levels of β-EP differ significantly from resting values. At the highest level of hyperglycemia (35 mM) β-EP was 3.1±0.2, 4.9±0.6 and 4.8±0.7 fmol·ml −1 in the resting, 2h and 48 h post exercise clamp studies respectively. The significance of these data is that this lack of a response is in distinct contrast to elevations of this peptide found during hypoglycemic states. We conclude that sustained hyperglycemia is not a stimulus to enhanced secretion of β-EP into plasma and this lack of a response is not effected by prior exercise.