Running is a popular form of exercise due to its health benefits and low economic cost; however, the prevalence of running-related injuries is on the rise. With most running injuries classified as overuse injuries due to excessive, repetitive loading, clinicians and researchers are looking to develop measures of this loading to assess a runner’s injury risk. One loading measure that is widely used due to its simplicity and ease of collection is loading rate. Loading rate is a measure of the change in the vertical force acting through a runner’s foot shortly after it comes in contact with the ground. Previous research findings are split on the effectiveness of loading rate as a measure of running injury risk. Some studies have found a relationship between high loading rate and injury, particularly bony stress fractures, while others have not. These inconsistent findings may be related to the varying methods used to calculate loading rate, as well as data collections occurring at different running speeds.

Our study of 139 male and female Division I NCAA cross country athletes is presented in the August 2022 issue of Medicine & Science in Sports & Exercise_®. We collected healthy, pre-season running mechanics and determined that loading rate values differ based on the calculation method used and the running speed of the collected data. We then monitored athletes for injury throughout the season and recorded 64 lower body injuries (e.g., muscle strains, tendinopathy) and 20 bony stress fractures. By comparing healthy, pre-season running mechanics of runners who remained healthy to runners who went on to sustain an injury, we determined that loading rate is not a significant predictor of in-season running injury, regardless of the method used to calculate loading rate.

Finding no relationship between loading rate during healthy running and subsequent injury indicates that loading rate is not an appropriate measure of running-injury risk. As loading rate is a simplified measure of the complex loading patterns experienced internally by the body during running, it is not surprising that a single force acting on the foot does not predict running injury. It is also important to remember that there are many factors (training volume, genetics, nutrition, running posture, etc.) contributing to a running injury, and a single biomechanical measure is unlikely to account for all these factors.

Clinically, loading rate-injury thresholds have been used to evaluate a runner’s injury risk. However, these thresholds should be used with caution as we found that they can only be compared to loading rate values calculated using the same calculation method and collected at the same running speed. More importantly, because we did not find an association between loading rate and injury, regardless of the calculation method used, using loading rate thresholds to predict injury could lead to inappropriate clinical decision-making and unnecessary treatment. It is therefore time to move past using loading rate as a predictor of running injury; we should instead focus our time and energy exploring alternative running measures and appreciating the complexity of running injuries by not limiting ourselves to a single biomechanical measure to predict injury. 

Christa M. Wille, DPT, received a doctorate in physical therapy from the University of Wisconsin-Madison. She went on to complete the UW Health Sports Residency program and is now working to complete her Ph.D. in biomedical engineering. Her research focus is on better understanding how muscle-strain injuries alter muscle microstructure and the resulting effects on muscular function and performance in the elite, intercollegiate population. In addition, she is also working with intercollegiate runners to better understand how running mechanics may predispose an athlete to a running-related injury. Clinically, Dr. Wille specializes in treating endurance athletes, especially runners.

Elizabeth Schmida recently completed a master’s degree in biomedical engineering at the University of Wisconsin-Madison. Now a research engineer in Badger Athletic Performance and the Neuromuscular Biomechanics Lab at UW-Madison, her work focuses on musculoskeletal modeling, particularly as it relates to running biomechanics. Her interests include running-gait mechanics and their association with running-related injury and wearable technology for human health and performance monitoring.

Viewpoints presented in SMB commentaries reflect opinions of the authors and do not necessarily represent ACSM positions or policies. Active Voice authors who have received financial or other considerations from a commercial entity associated with their topic must disclose such relationships at the time they accept an invitation to write for SMB.

Cancer-related fatigue (C-rF) is a debilitating symptom that affects around one-third of people for months or years after cancer treatment. While the etiology of C-rF remains uncertain, it has been demonstrated that cancer survivors with C-rF display impaired exercise tolerance compared with those without C-rF, with the degree of exercise intolerance associated with chronic fatigue severity. Exercise intolerance in cancer survivors with C-rF likely contributes to reported difficulties in performing activities of daily living, as well as impaired quality of life. Thus, understanding the physiological (e.g., cardiopulmonary, metabolic and neuromuscular) alterations contributing to impaired exercise tolerance in people with C-rF is of importance, particularly given that these impairments could be reversible through exercise training.

One physiological alteration that could hinder the ability to perform activities of daily living is neuromuscular fatigability, defined as the reduction in neuromuscular function in response to exercise. To gain a better understanding of the etiology of neuromuscular fatigability in cancer survivors with C-rF, our study, published in Medicine and Science in Sports and Exercise_®, assessed the mechanisms of neuromuscular fatigability in cancer survivors with and without C-rF. We recruited 96 cancer survivors and separated the participants into two groups (fatigued and non-fatigued) based on a clinical cut-point for the diagnosis of chronic fatigue. In response to incremental cycling stages interspersed with measures of neuromuscular function, neuromuscular fatigability was assessed through changes in maximal voluntary contraction force of the knee extensors. The mechanisms of reduced maximal contraction force were determined through electrical stimulations either superimposed to voluntary contractions (capacity of the nervous system to activate muscle) or evoked on relaxed muscles (their contractility). Moreover, power outputs during cycling were expressed relative to gas exchange thresholds to determine the relative intensity of exercise.

Our results demonstrated that the magnitude and rate of decrements in neuromuscular function was substantially greater in the fatigued versus non-fatigued group. For example, following just 3 minutes of exercise at a low absolute (~20-25 W) and relative power output (47% of the gas exchange threshold), the fatigued group demonstrated decrements to maximal muscle force generating capacity that were five times greater than the non-fatigued group (−10% vs −2% on average, respectively). The responses to electrically evoked contractions revealed that mechanisms residing in the muscle were primarily responsible for the greater fatigability in the fatigued group.

The rapid and profound decrements in neuromuscular function we found in response to low-intensity exercise in those with C-rF was striking. Such a rapid decline in neuromuscular function in response to exercise of low power output has potentially important implications for the physiological and perceptual impact of typical activities of daily living. For example, the low intensity during the initial stages of cycling is likely to correspond with activities such as walking, housework, gardening or slowly climbing stairs. Accordingly, impaired neuromuscular fatigability, owing to rapid perturbations in the muscle, might represent an important contributor to the regularly reported difficulties in performing physical tasks of daily living in those with C-rF.

Dr. Callum Brownstein (@CGBrownstein) is a postdoctoral researcher at University Jean Monnet, Saint Etienne, France. He completed his Ph.D. at Northumbria University, Newcastle, U.K., where he assessed recovery of neuromuscular function following high-intensity intermittent exercise. His current research focuses on the acute integrative response to whole-body exercise in athletes, healthy active and clinical populations, with a focus on neuromuscular perturbations.

Dr. Guillaume Millet (@kinesiologui) is a professor of exercise physiology at University Jean Monnet, Saint-Etienne, France. After graduating from the University of Franche-Comte in 1997, he held various positions in Dijon, Saint-Etienne and Grenoble. Between 2013 and 2018, he was professor in the Human Performance Laboratory and the Faculty of Kinesiology at the University of Calgary (Canada), where he led a research group on neuromuscular fatigue. In 2019, he was named at the Institut Universitaire de France as a senior member. His general research area investigates the physiological, neurophysiological and biomechanical factors associated with fatigue, both in extreme exercise (ultra-endurance) and patients (neuromuscular diseases, cancer, multiple sclerosis, ICU).

Viewpoints presented in SMB commentaries reflect opinions of the authors and do not necessarily represent ACSM positions or policies. Active Voice authors who have received financial or other considerations from a commercial entity associated with their topic must disclose such relationships at the time they accept an invitation to write for SMB.

In our Studies of Twin Responses to Understand Exercise THerapy (STRUETH) trial, we recruited monozygotic and dizygotic twin pairs and supervised them through three months of endurance training and three months of resistance exercise training. Each twin pair exercised together, at matched exercise prescriptions, and all subjects undertook both forms of exercise. We measured many outcomes, including body composition, fitness and strength, risk factors and vascular measures, but one of the most interesting outcomes involved cardiac magnetic resonance (CMR) assessments of heart chamber mass and volumes.

Not everyone responds to exercise in the same way, even when identical programs are administered. Thus, we were curious about the variability between individuals (and twin pairs) in heart muscle adaptation to training, and whether the modality of training affected this. An early study by Morganroth and colleagues in 1975 assessed different types of athletes, using the rudimentary echocardiography of that time, and reported distinct cardiac morphological findings between groups. From this grew the notion that endurance training induces eccentric hypertrophy (where ventricular volumes and mass increase), whereas resistance training leads to concentric hypertrophy (where mass and wall thicknesses increase, but volumes do not). But the original paper, and some that followed and supported the hypothesis, did not actually exercise-train the subjects. Rather, comparisons were cross-sectional and assumed that group differences were due to lifelong exercise exposure. However, athletes differ greatly in many ways, including body size and shape.

Our study, published in the July 2022 issue of Medicine & Science in Sports & Exercise_®, provides further insight. Using CMR, we found evidence for increased left ventricular mass and volume in response to endurance training, supporting the idea of eccentric hypertrophy. Somewhat in contrast, resistance training in the same individuals did not modify left ventricular dimensions or mass. This brings into question the proposition that resistance training induces concentric hypertrophy. By looking at the individual responses, we were able to quantify the proportion of the sample with large, modest and nonresponse to each modality of training. These data showed that low responders to one mode of exercise were often high responders to the alternative!

The modes of exercise we used were very different, targeting cardiovascular function versus skeletal muscle hypertrophy. They might therefore be expected to induce changes in distinct gene subsets. Perhaps individuals are genetically predisposed to respond to one or other forms of training? However, our estimates based on actual changes induced by training indicated limited genetic impact on cardiac adaptation to either mode of training.

Like all studies, ours has some limitations. The training period was relatively short, different exercise interventions may induce other outcomes, and the subjects were young and healthy (though initially inactive). Our power for twin analysis was somewhat limited, especially in the dizygotic paired groups. Interestingly, 10 pairs of twins who were recruited to the dizygotic group based on their lifelong assumptions turned out to be monozygotic when we genotyped them. Few previous twin studies have genotyped their sample to verify zygosity — our data suggest that this is necessary in future.

Our findings provide further insight into the ongoing debate regarding the utility of searching for genetic determinants of trainability in humans. At the end of the day, most people respond to some form of exercise — the challenge for exercise physiologists remains to fit the best approach to each individual.

Daniel J. Green, Ph.D., is a cardiovascular physiologist who studies exercise, inactivity, and cardiovascular function and adaptation in humans. His research has encompassed the development of new imaging platforms to study the impact of lifestyle factors (particularly exercise) on human adaptation across the lifespan. Dr. Green is Winthrop Professor in Sport and Exercise Science at the University of Western Australia, and this work was completed during his tenure as a National Health and Medical Research Council of Australia (NHMRC) principal research fellow (APP1080914).

Louise Naylor, Ph.D., is an associate professor at the University of Western Australia and a senior accredited exercise physiologist who works in cardiac rehabilitation in the Cardiac Transplant Unit and Advanced Heart Failure Service at Fiona Stanley Hospital. As both a practitioner and researcher, Dr. Naylor aims to optimize the prescription of exercise for people both at risk of and with established cardiovascular diseases.

Viewpoints presented in SMB commentaries reflect opinions of the authors and do not necessarily represent ACSM positions or policies. Active Voice authors who have received financial or other considerations from a commercial entity associated with their topic must disclose such relationships at the time they accept an invitation to write for SMB.