An Investigation of Exercise-Induced Hypoalgesia After Isometric and Cardiovascular Exercise

Exercise-induced hypoalgesia is a well-established phenomenon in the literature. The underlying mechanisms responsible for this augmentation of pain perception are not completely understood. The specific mode and intensity of exercise that creates hypoalgesia remains equivocal. Therefore, the purpose of this study was to identify if any differences existed in the exercise-induced hypoalgesia of isometric gripping exercise (IGE) and treadmill exercise (TE). A repeated measures design was used to determine the differences in pain threshold between acute exposure to IGE and TE. Twelve healthy male volunteers served as our subjects. Subjects were tested on three different days under three different conditions (rest, IGE, TE). The order of the trials was randomized and applied force (AF) was used as the dependent variable. Applied force pain threshold (AFPT) was determined by a handheld dolorimeter used to apply progressive force and pain to the skin and muscles of the wrist flexors before and after exercise. Exercise induced hypoalgesia was found in both exercise conditions by comparing resting PPT values (6.23 ± 2.04) to those measured immediately after IGE (7.24 ± 1.61; p = 0.0058) or TE (8.03 ± 2.03; p = 0.0001). However, TE produced a larger (22.04 %) hypoanalgesic effect in comparison to isometric exercise (14.14 %). Both TE and IGE may have potential as methods of increasing one’s pressure pain threshold. Further investigation into the specific causes of exercise-induced hypoalgesia is warranted

Muscle Damage following Maximal Eccentric Knee Extensions in Males and Females

Aim: To investigate whether there is a sex difference in exercise induced muscle damage. Materials and Method: Vastus Lateralis and patella tendon properties were measured in males and females using ultrasonography. During maximal voluntary eccentric knee extensions (12 reps x 6 sets), Vastus Lateralis fascicle lengthening and maximal voluntary eccentric knee extensions torque were recorded every 10° of knee joint angle (20–90°). Isometric torque, Creatine Kinase and muscle soreness were measured pre, post, 48, 96 and 168 hours post damage as markers of exercise induced muscle damage. Results: Patella tendon stiffness and Vastus Lateralis fascicle lengthening were significantly higher in males compared to females (p0.05). Creatine Kinase levels post exercise induced muscle damage were higher in males compared to females (p<0.05), and remained higher when maximal voluntary eccentric knee extension torque, relative to estimated quadriceps anatomical cross sectional area, was taken as a covariate (p<0.05). Conclusion: Based on isometric torque loss, there is no sex difference in exercise induced muscle damage. The higher Creatine Kinase in males could not be explained by differences in maximal voluntary eccentric knee extension torque, Vastus Lateralis fascicle lengthening and patella tendon stiffness. Further research is required to understand the significant sex differences in Creatine Kinase levels following exercise induced muscle damage

Effects of exercise-induced arterial hypoxemia on limb muscle fatigue and performance

1. Reductions in arterial O2 saturation (−5% to −10% SaO2 below rest) occur over time during sustained heavy-intensity exercise in a normoxic environment, caused primarily by the effects of acid pH and increased temperature on the position of the HbO2 dissociation curve. 2. We prevented the desaturation incurred during exercise at ∼90% √O2 MAX via increased fraction of inspired O2 (FiO2) (0.23 to 0.29) and showed that exercise time to exhaustion was increased. 3. We used supramaximal magnetic stimulation (1–100 Hz) of the femoral nerve to test for quadriceps fatigue. We used mildly hyperoxic inspirates (FiO2 0.23 to 0.29) to prevent O2 desaturation. We then compared the amount of quadriceps fatigue incurred following cycling exercise at SaO2 91% vs 98% with each trial carried out at identical work rates and for equal durations. 4. Preventing the normal exercise-induced O2 desaturation prevented about one-half the amount of exercise-induced quadriceps fatigue; plasma lactate and effort perception were also reduced. In a subset of less fit subjects who showed only minimal arterial hypoxaemia during sustained exercise (SaO2 ∼95%), breathing a mildly hypoxic inspirate (FiO2 0.17; SaO2 ∼88%) exacerbated the quadriceps fatigue. 5. We conclude that the normal exercise-induced O2 desaturation during heavy-intensity endurance exercise contributes significantly to exercise performance limitation in part because of its effect on locomotor muscle fatigue

Exercise-induced respiratory muscle fatigue: implications for performance

It is commonly held that the respiratory system has ample capacity relative to the demand for maximal O-2 and CO2 transport in healthy humans exercising near sea level. However, this situation may not apply during heavy-intensity, sustained exercise where exercise may encroach on the capacity of the respiratory system. Nerve stimulation techniques have provided objective evidence that the diaphragm and abdominal muscles are susceptible to fatigue with heavy, sustained exercise. The fatigue appears to be due to elevated levels of respiratory muscle work combined with an increased competition for blood flow with limb locomotor muscles. When respiratory muscles are prefatigued using voluntary respiratory maneuvers, time to exhaustion during subsequent exercise is decreased. Partially unloading the respiratory muscles during heavy exercise using low-density gas mixtures or mechanical ventilation can prevent exercise-induced diaphragm fatigue and increase exercise time to exhaustion. Collectively, these findings suggest that respiratory muscle fatigue may be involved in limiting exercise tolerance or that other factors, including alterations in the sensation of dyspnea or mechanical load, may be important. The major consequence of respiratory muscle fatigue is an increased sympathetic vasoconstrictor outflow to working skeletal muscle through a respiratory muscle metaboreflex, thereby reducing limb blood flow and increasing the severity of exercise-induced locomotor muscle fatigue. An increase in limb locomotor muscle fatigue may play a pivotal role in determining exercise tolerance through a direct effect on muscle force output and a feedback effect on effort perception, causing reduced motor output to the working limb muscles

Exercise Intensity as a Determinant of Exercise Induced Hypoalgesia

The purpose of this study was to examine pain perception during and following two separate 30-min bouts of exercise above and below the Lactate Threshold (LT). Pain Threshold (PT) and Pain Intensity (PI) were monitored during (15 and 30 min) and after exercise (15 and 30 min into recovery) using a Cold Pressor Test (CPT) and Visual Analog Scale (VAS) for pain of the non-dominant hand. Significant differences in PT scores were found both during and after exercise conditions. Post hoc analysis revealed significant differences in PT scores at 30 min of exercise (P=0.024, P=0.02) and 15 min of recovery (P=0.03, P=0.01) for exercise conditions above and below LT, respectively. No differences (P=0.05) in PT scores were found at any time point between exercise conditions. No differences were found in PI scores at any time point within each trial (P=0.05) as well as between exercise conditions (p=0.05). Based upon these data, the effects of moderate exercise on PT appear to be similar at exercise intensities just above and below LT. This may indicate that the requisite intensity needed to ellicit Exercise-Induced Hypoalgesia may be lower than previously reported. Because a hypoalgesic effect was not observed in either condition until 30 min of exercise had been completed, total exercise time may be an important factor in the augmentation of pain perception under these conditions

Severe bronchial asthma in children with exercise-induced bronchospasm

Based on a complex examination 46 of schoolchildren suffering from severe asthma, we established that greater proportion of schoolchildren with exercise-induced asthma was with symptoms of mucospin hypereosinophilia (average content of eosinophilic granulocytes over 8 %) than children suffering from severe type of the disease, with no signs of exercise-induced bronchoconstriction. The bronchi of the schoolchildren with severe exercise-induced bronchial asthma are hyperresponsive to histamine, significantly greater proportion of patients with severe airway hypersensitivity to histamine (PC20H<0,5 mg/ml) among the children exercise-induced asthma than those without phenomena of exercise-induced constriction

Influence of exercise-induced energy deficit on non-exercise activity thermogenesis in overweight and obese adults

Energy balance is a dynamically regulated system and perturbing one of its components (reduction in energy intake (EI) or increase in energy expenditure (EE)) can result in biological and behavioural compensatory responses of unpredictable magnitude elsewhere in the system. In fact, exercise-induced EE can elicit compensatory changes in EI and/or non-exercise activity thermogenesis (NEAT), which consequently attenuate theenergy gap between EI and EE. Although compelling evidence suggests that exercise mediated changes in NEAT seem to be subject to large inter-individual variance, research investigating the impact of biological sex on exercise-induced modulation of NEAT is lacking. Therefore, the aim of this study was to investigate the effect of an exercise induced energy deficit on NEAT in overweight and obese men and women

Conditioned Pain Modulation Predicts Exercise-Induced Hypoalgesia in Healthy Adults

Introduction: Conditioned pain modulation (CPM) is the concept that pain inhibits pain and has potential rehabilitation implications for exercise prescription. The purpose of this study was to determine whether changes in pressure pain perception after a thermal conditioning stimulus (i.e., CPM) was attenuated with aging and whether CPM predicted pain relief after exercise (exercise-induced hypoalgesia (EIH)) in healthy young and older adults. Methods: Twenty young (21.9 ± 3.3 yr, 10 men) and 19 older (72.0 ± 4.5 yr, 10 men) adults participated in three sessions: one familiarization and two experimental (EIH and CPM) sessions. Pressure pain perception was assessed using a weighted Lucite edge placed on the right index finger for 1 min. EIH was determined by measuring pressure pain perception before and after prolonged submaximal isometric contraction of the elbow flexors. CPM was assessed by measuring pressure pain perception at the finger while the foot was immersed in neutral water versus painful ice water. Results: Young, but not older, adults reported a decrease in pressure pain at the finger while their foot was immersed in the ice water bath compared with the neutral bath (i.e., CPM, trial–age: P = 0.001). Pressure pain ratings decreased after exercise (P = 0.03) that was perceived as painful (peak arm pain, 7.0 ± 3.3) for both young and older adults. Regression analysis showed that after controlling for age and baseline pain, CPM predicted EIH (model adjusted R2 = 0.23, P = 0.007). Conclusions: CPM was attenuated in older adults, as measured with a noxious pressure stimulus after a thermal conditioning stimulus, and adults with greater CPM were more likely to report greater EIH

Sex differences in exercise-induced diaphragmatic fatigue in endurance-trained athletes

There is evidence that female athletes may be more susceptible to exercise-induced arterial hypoxemia and expiratory flow limitation and have greater increases in operational lung volumes during exercise relative to men. These pulmonary limitations may ultimately lead to greater levels of diaphragmatic fatigue in women. Accordingly, the purpose of this study was to determine whether there are sex differences in the prevalence and severity of exercise-induced diaphragmatic fatigue in 38 healthy endurance-trained men (n = 19; maximal aerobic capacity = 64.0 ± 1.9 ml·kg–1·min–1) and women (n = 19; maximal aerobic capacity = 57.1 ± 1.5 ml·kg–1·min–1). Transdiaphragmatic pressure (Pdi) was calculated as the difference between gastric and esophageal pressures. Inspiratory pressure-time products of the diaphragm and esophagus were calculated as the product of breathing frequency and the Pdi and esophageal pressure time integrals, respectively. Cervical magnetic stimulation was used to measure potentiated Pdi twitches (Pdi,tw) before and 10, 30, and 60 min after a constant-load cycling test performed at 90% of peak work rate until exhaustion. Diaphragm fatigue was considered present if there was a 15% reduction in Pdi,tw after exercise. Diaphragm fatigue occurred in 11 of 19 men (58%) and 8 of 19 women (42%). The percent drop in Pdi,tw at 10, 30, and 60 min after exercise in men (n = 11) was 30.6 ± 2.3, 20.7 ± 3.2, and 13.3 ± 4.5%, respectively, whereas results in women (n = 8) were 21.0 ± 2.1, 11.6 ± 2.9, and 9.7 ± 4.2%, respectively, with sex differences occurring at 10 and 30 min (P < 0.05). Men continued to have a reduced contribution of the diaphragm to total inspiratory force output (pressure-time product of the diaphragm/pressure-time product of the esophagus) during exercise, whereas diaphragmatic contribution in women changed very little over time. The findings from this study point to a female diaphragm that is more resistant to fatigue relative to their male counterparts

Exercise-induced whole-body dehydration does not affect airway responsiveness in athletes but may impair small airway function

Exercise-induced bronchoconstriction (EIB) is the transient narrowing of the airways that occurs during or shortly after strenuous exercise. Loss of water from the airway surface, due to the conditioning of large volumes of air during exercise, is the main physiological stimulus for EIB. We proposed that exercise-induced whole-body dehydration would interfere with hydration of the airways and, consequently, increase the risk and/or severity of EIB. We also investigated the effects of whole-body dehydration on resting lung function