Jens Halkjær-Kristensen

A mechanism for increased contractile strength of human pennate muscle in response to strength training: changes in muscle architecture

1 In human pennate muscle, changes in anatomical cross‐sectional area (CSA) or volume caused by training or inactivity may not necessarily reflect the change in physiological CSA, and thereby in maximal contractile force, since a simultaneous change in muscle fibre pennation angle could also occur. 2 Eleven male subjects undertook 14 weeks of heavy‐resistance strength training of the lower limb muscles. Before and after training anatomical CSA and volume of the human quadriceps femoris muscle were assessed by use of magnetic resonance imaging (MRI), muscle fibre pennation angle (θp) was measured in the vastus lateralis (VL) by use of ultrasonography, and muscle fibre CSA (CSAfibre) was obtained by needle biopsy sampling in VL. 3 Anatomical muscle CSA and volume increased with training from 77.5 ± 3.0 to 85.0 ± 2.7 cm2 and 1676 ± 63 to 1841 ± 57 cm3, respectively (±s.e.m.). Furthermore, VL pennation angle increased from 8.0 ± 0.4 to 10.7 ± 0.6 deg and CSAfibre increased from 3754 ± 271 to 4238 ± 202 μm2. Isometric quadriceps strength increased from 282.6 ± 11.7 to 327.0 ± 12.4 N m. 4 A positive relationship was observed between θp and quadriceps volume prior to training (r = 0.622). Multifactor regression analysis revealed a stronger relationship when θp and CSAfibre were combined (R= 0.728). Post‐training increases in CSAfibre were related to the increase in quadriceps volume (r = 0.749). 5 Myosin heavy chain (MHC) isoform distribution (type I and II) remained unaltered with training. 6 VL muscle fibre pennation angle was observed to increase in response to resistance training. This allowed single muscle fibre CSA and maximal contractile strength to increase more (+16 %) than anatomical muscle CSA and volume (+10 %). 7 Collectively, the present data suggest that the morphology, architecture and contractile capacity of human pennate muscle are interrelated, in vivo. This interaction seems to include the specific adaptation responses evoked by intensive resistance training.

Exercise-induced increase in serum interleukin-6 in humans is related to muscle damage.

1. This study was performed to test the hypothesis that the exercise‐induced increase in circulating cytokine levels is associated with muscle damage. Nine healthy young male subjects performed two high‐intensity bicycle exercise trials separated by two weeks. The first trial consisted of 30 min of normal bicycle exercise (concentric exercise), whereas the second consisted of 30 min of braking with reversed revolution (eccentric exercise). The work loads were chosen to give the same increases in heart rate and catecholamine levels in the blood during each trial. 2. Significant increases (P < 0.05) in plasma concentration of creatine kinase (CK), aspartate aminotransferase and alanine aminotransferase were observed only after the eccentric exercise. Furthermore, the level of interleukin‐6 (IL‐6) in serum increased significantly after the eccentric exercise and was significantly correlated to CK concentration in the following days, whereas no significant changes were found after the concentric exercise. 3. The total concentration of lymphocytes increased significantly (P < 0.05) as a result of eccentric compared with concentric exercise. This was mainly due to a significantly more pronounced recruitment of natural killer (NK) cells and CD8 positive cells (CD8+ cells) during the eccentric trial. However, no significant differences between the two types of work were found in regard to the circulating concentration of monocytes. The concentration of neutrophils was only significantly increased 2 h after the concentric exercise. 4. The finding that high‐intensity eccentric exercise caused a more pronounced increase in the plasma level of IL‐6, compared with concentric exercise, supports the hypothesis that the post‐exercise cytokine production is related to skeletal muscle damage. The fact that no differences between eccentric and concentric exercise were found in the recruitment of most blood mononuclear cell subsets to the blood supports the hypothesis that the exercise‐induced increase in plasma catecholamines is a major determinant of the mobilization of these cells into the blood. However, as eccentric exercise caused a more pronounced increase in the concentration of NK cells and CD8+ cells, factors involved in muscle damage may also contribute to the recruitment of these cells.

Modulation of natural killer cell activity in peripheral blood by physical exercise.

The present study was designed to examine the effect of physical exercise on human natural killer (NK) cells. Six healthy volunteers underwent two different acute physical exercise tests with an interval of at least 1 week: (1) 60min bicycle exercise at 80% of maximal oxygen uptake (VO2max) and (2) 60 min back‐muscle training at up to 29% of VO2max; blood samples were collected before and during the last few minutes of exercise, as well as 2 h and 24 h afterwards. The NK cell activity (lysis/fixed number of mononuclear cells) increased during bicycle exercise, dropped to a minimum 2 h later and returned to pre‐exercise levels within 24 h. Back‐muscle exercise did not significantly influence NK cell activity. Plasma levels of adrenaline, noradrenaline, and cortisol were elevated during bicycling, but not during back‐muscle exercise, indicating that exercise intensity is a determinant of NK cell activity. During bicycle exercise the NK cell subset (CD 16+ cells) of mononuclear cells increased significantly. Furthermore an improved interleukin 2 (IL‐2) boosting of the NK cell activity was found during work as compared to IFN‐α and indomethacin‐enhanced NK cell activity. These results indicate that NK cells with a high IL‐2 response capacity are recruited to the peripheral blood during exercise. The decreased NK cell activity demonstrated 2 h after work was probably not due to fluctuations in size of the NK cell pool, since the proportion of CD16+ cells was normal. The finding that indomethacin fully restored the suppressed NK cell activity in vitro and the demonstration of a twofold increase in monocyte (CD20+ cells) proportions 2 h after work, strongly indicate that prostaglandins released by monocytes during the heavy physical exercise are responsible for the down‐regulation of the NK cells.

Effect of Physical Exercise on Blood Mononuclear Cell Subpopulations and in Vitro Proliferative Responses

The present study was designed to examine the effect of physical exercise on subsets and proliferative responses of blood mononuclear cells. Sixteen young, healthy volunteers underwent 60min of bicycle exercise at 75% of maximal oxygen uptake (VO2max). After an interval of at least 1 week, six of the subjects underwent a 60‐min back muscle training period at up to 30% of VO2max. Blood samples were collected before and during the last minutes of exercise, as well as 2 and 24 h later. Blood mononuclear cell (BMNC) subpopulations were determined and the proliferate responses after incubation with phytohaemagglutinin (PHA) or purified derivative of tuberculin (PPD), were quantified by [3H]thymidine incorporation. During bicycle exercise the relative blood concentration of T cells (CD3+ cells) declined, mainly due to a fall in T helper cells (CD4+ cells). The natural killer (NK) cell subset (CD16+ cells) increased during work, but reverted after; the monocytes (CD14+ cells) increased 2 h after work, whereas the B‐cell subset (CD20+ cells) did not change. BMNC subsets were not significantly changed by back muscle exercise. The PHA‐induced proliferative response decreased during bicycle exercise, whereas the PPD‐induced response did not change. No significant changes occurred during back muscle exercise. Investigation of subgroups after incubation with [3H]thymidine showed that the proliferative response per CD4+ cell did not change in relation to exercise, but the contribution of the CD4+ subgroup to proliferation declined during bicycle exercise due to the decreased proportion of CD4+ cells. The suppression of the PHA response during bicycle exercise can be explained in part by a relative fall in CD4+ cells. The pool sizes of BMNC subfraction may be elicited by increased catecholamine and cortisol levels.

Exercise induces recruitment of lymphocytes with an activated phenotype and short telomeres in young and elderly humans.

This study was performed in order to investigate the type of T cells recruited to the blood in response to an acute bout of exercise with regard to mean lengths of telomeric terminal restriction fragments (TRF) and surface activation markers and with special emphasis on age-associated differences. Ten elderly and ten young humans performed maximal bicycle exercise. There was no difference in the number of recruited CD4+ and CD8+ cells between the young and elderly group. In both age groups the immediate increases could be ascribed to recruitment of CD28- cells (CD8+ and CD4+ cells) and memory cells (only CD8+ cells). Furthermore, after exercise mean TRF lengths were significantly reduced in blood mononuclear cells and in CD8+ cells from young subjects and in CD4+ cells from elderly subjects compared with lengths pre-exercise. These findings suggest that the mobilization of T lymphocytes during acute exercise is mainly a redistribution of previously activated cells with an increased replicative story than cells isolated from the blood at rest. Furthermore, elderly humans fulfilling the Senieur protocol have a preserved ability to recruit T lymphocytes in response to acute physical stress.

Impaired thermoregulation in adults with growth hormone deficiency during heat exposure and exercise

OBJECTIVE It has recently been shown that patients with growth hormone deficiency have a reduced sweating capacity. We hypothesize that reduced sweating might affect thermoregulation in growth hormone deficiency patients. In the present study we have examined thermoregulation in growth hormone deficiency patients.

Variations in single fibre areas and fibre composition in needle biopsies from the human quadriceps muscle

Cross-sectional area of a single fibres and the fibre distribution were measured for the two main types of fibres in needle biopsies from the quadriceps muscle of ten healthy young males. Methodological errors expressed as coefficient of variation (CV) of a single value for the area measurements were analysed and found to be 2.4% including the intraindividual error in handling the planimeter. An inhomogeneity in distribution and size of the fibres within the quadriceps muscle was indicated by a CV within the same section of 6-8% and between repeated biopsies of 15-20%.

Maximal oxygen consumption rate in patients with bronchial asthma—the effect of β2-adrenoreceptor stimulation

Five young male patients with exercise-induced asthma (EIA) were subjected to graded bicycle exercise with work loads corresponding to 50%, 75% and 120% of the load necessary to elicit maximal oxygen uptake (Vo2 max). The exercise tests were performed after inhalation of salbutamol (Ventoline) as well as after inhalation of saline as control. Additionally two maximal work tests (bicycling and treadmill) were performed without inhalation on a work load corresponding to 100% Vo2 max. Oxygen uptake (Vo2) heart rate (HR), mean blood pressure (MBP), rating of perceived exertion (RPE) as well as arterial concentration of glucose and acid-base variables were measured. Vo2 max during bicycle exercise averaged 3.16 l/min and no significant difference was disclosed between the beta 2-stimulation and the control situations. The coefficient of variation of a single Vo2 max measurement was 4.7%. The maximal treadmill running revealed a significantly higher Vo2 max (3.42 l/min, P less than 0.05) than during bicycling; no EIA was provoked in any of the experiments. After beta 2-stimulation a higher HR and MBP in relation to Vo2 was observed than in the control experiment; however, the slope of HR/Vo2 and MBP/Vo2 relationships was not affected. Normal relationships were observed between Vo2 and work load, ventilation, RPE and acid-base data and these relations were unaffected of beta 2-stimulation. It is concluded, that Vo2 max seems to be within the normal range in asthmatics, provided they are free from attacks.

Effect of physical training on peak oxygen consumption rate and exercise-induced asthma in adult asthmatics

Sixteen adults with perennial asthma were trained for 2 months using heavy exercise. Eleven comparable subjects performing light exercise with the same frequency and duration served as controls. After the training the peak oxygen consumption rate (Vo2max) was increased by 10% (P = 0.02) in the heavily trained group, whereas no significant change was observed in the control group. The difference in Vo2max between males and females averaged 20% and is thus of the same magnitude as found in healthy subjects. An exercise-induced asthma (EIA) test comprising 6 min of free running was carried out in all participants in both training groups before and after the training period. The post-exercise decrease in pulmonary function assessed by peak expiratory flow (PEF) was 36 + 4% (mean +/- SEM) before heavy training and 33 +/- 2% after two months of training (paired t-test: P = 0.18); for the control group the decrease was 40 +/- 6% and 40 +/- 7% (P = 0.22), respectively, at the pre- and post-training investigation. It is concluded that physical training may increase the Vo2max in asthmatic patients by the same amount as in normal subjects, whereas no influence on the degree of EIA could be detected.

SHORT-TERM PHYSICAL TRAINING IN BRONCHIAL ASTHMA

The effect of two types of physical training on patients with perennial asthma were compared in a blind, controlled, randomized study. Eleven of 27 adults with asthma performed a physical training programme which did not change their oxygen consumption (control group). The remaining 16 asthmatics performed a physical training programme which improved their maximal oxygen consumption (training group). Both of the training programmes were performed for 1 hour, twice a week during a period of 2 months. No complications were reported during the performance of the training programmes. The doses of all medicines apart from beta 2-agonist aerosol were unchanged during the training period. The patients inhaled beta 2-agonist aerosol if their peak expiratory flow (PEF) was less than 60% of their maximal PEF. The training group decreased their use of aerosol from an average of 4.94 puffs per day to 3.41 puffs per day (P less than 0.05). The control group did not change their use of beta 2-agonist aerosol significantly. It is concluded that physical exercise which improves the maximal oxygen consumption decreases the use of beta 2-agonist spray and that heavy exercise is well tolerated by asthmatics.