Register or Submit a manuscript.
Quick Link
OBM Geriatrics

(ISSN 2638-1311)

OBM Geriatrics is an international peer-reviewed Open Access journal published quarterly online by LIDSEN Publishing Inc. The journal takes the premise that innovative approaches – including gene therapy, cell therapy, and epigenetic modulation – will result in clinical interventions that alter the fundamental pathology and the clinical course of age-related human diseases. We will give strong preference to papers that emphasize an alteration (or a potential alteration) in the fundamental disease course of Alzheimer’s disease, vascular aging diseases, osteoarthritis, osteoporosis, skin aging, immune senescence, and other age-related diseases.

Geriatric medicine is now entering a unique point in history, where the focus will no longer be on palliative, ameliorative, or social aspects of care for age-related disease, but will be capable of stopping, preventing, and reversing major disease constellations that have heretofore been entirely resistant to interventions based on “small molecular” pharmacological approaches. With the changing emphasis from genetic to epigenetic understandings of pathology (including telomere biology), with the use of gene delivery systems (including viral delivery systems), and with the use of cell-based therapies (including stem cell therapies), a fatalistic view of age-related disease is no longer a reasonable clinical default nor an appropriate clinical research paradigm.

Precedence will be given to papers describing fundamental interventions, including interventions that affect cell senescence, patterns of gene expression, telomere biology, stem cell biology, and other innovative, 21st century interventions, especially if the focus is on clinical applications, ongoing clinical trials, or animal trials preparatory to phase 1 human clinical trials.

Papers must be clear and concise, but detailed data is strongly encouraged. The journal publishes a variety of article types (Original Research, Review, Communication, Opinion, Comment, Conference Report, Technical Note, Book Review, etc.). There is no restriction on the length of the papers and we encourage scientists to publish their results in as much detail as possible.

 
 

Publication Speed (median values for papers published in 2024): Submission to First Decision: 6.3 weeks; Submission to Acceptance: 11.4 weeks; Acceptance to Publication: 7 days (1-2 days of FREE language polishing included)

 
 
Current Issue: 2026  Archive: 2025 2024 2023 2022 2021 2020 2019 2018 2017
Open Access Short Review

Maximal 4-Second Cycle Accelerations Attenuate Sarcopenia and Improve Cardiovascular Function in Older Adults

Edward F. Coyle *

  1. The Human Performance Laboratory, Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, TX 78712, USA

* Correspondence: Edward F. Coyle

Academic Editor: Daniel A. Traylor

Special Issue: A Proactive Approach to Sarcopenia in Aging Populations

Received: February 20, 2025 | Accepted: July 28, 2025 | Published: August 08, 2025

OBM Geriatrics 2025, Volume 9, Issue 3, doi:10.21926/obm.geriatr.2503320

Recommended citation: Coyle EF. Maximal 4-Second Cycle Accelerations Attenuate Sarcopenia and Improve Cardiovascular Function in Older Adults. OBM Geriatrics 2025; 9(3): 320; doi:10.21926/obm.geriatr.2503320.

© 2025 by the authors. This is an open access article distributed under the conditions of the Creative Commons by Attribution License, which permits unrestricted use, distribution, and reproduction in any medium or format, provided the original work is correctly cited.

Abstract

The shrinkage of muscles with age, beginning at 30 y and accelerating in old age, is due largely to atrophy of fast-twitch muscle fibers (FT) partly from disuse. It was our purpose to develop an exercise program that is effective and time efficient at stimulating FT, as well as slow-twitch fibers (ST), to offset their atrophy. FT are recruited during movements requiring very high force and/or high velocity. We developed a safe exercise cycle that allows a person to ‘accelerate’ with the maximal effort needed to recruit the highest number of ST and especially FT fibers. ‘Inertial Loading’ allows the person to maximally accelerate the cycle flywheel through the full range of the force vs. velocity relationship (0-160 RPM), and accurately identifies maximal power (Pmax), which can be used to diagnosis muscle loss. Of note, Pmax is usually five-fold higher than the power encountered during any aerobic exercise or ‘High Intensity Interval Training (HIIT)’. The very high Pmax serves as a very potent stimulator of the muscle, the nervous system and the cardiovascular system. This remarkably reduces the total exercise time (1-2 minutes) needed in a 10-minute workout, which is comprised of repeated 4-second accelerations and 15-45 seconds of recovery. The 4-seconds of maximal acceleration robustly activate FT, based on increases in mRNA from genes and pathways involved in muscle hypertrophy. Furthermore, NASA experiments used these cycle accelerations during 70 days of bed rest, that simulates muscle atrophy with space flight but also aging. NASA reported that performing 24 seconds (4 s × 6) of maximal acceleration cycling every 8 days, along with less frequent short bouts of aerobic exercise, totally prevented the normally large atrophy of FT, and it reduced the whole muscle atrophy by one-half. Specifically, when older adults train with maximal accelerations for 8 weeks, they display significant hypertrophy of their thigh muscles, increases in maximal power, and better performance in tasks of daily living. The cardiovascular system also improves function with these repeated high-power sprints and short rest, with significant increases in heart function, maximal oxygen consumption and arterial elasticity. Therefore, performing repeated maximal 4-second accelerations on an inertially loaded cycle ergometer, beginning at 30 y and continuing throughout old age, has promise to be a safe and viable proactive treatment to both diagnosis and counteract the progression of muscle wasting, sarcopenia and reduced cardiovascular function.

Keywords

Sarcopenia; muscle power; hypertrophy

1. Introduction

This manuscript is meant to be proactive in proposing an ideal exercise regime for attenuating the loss of muscle mass with age and offsetting sarcopenia. People commonly show more than a 30-40% decline in muscle mass with greater reductions in strength and function by the age of 75 years [1,2,3,4]. It has been reported that 13-24% of 70-year-olds, and more than 50% of all people surveyed over 80 years, have sarcopenia, although diagnostic standards vary and remain ill-defined. The loss of muscle mass, strength, and power with advancing age, begins in the third to fourth decade [3,4]. Strength and maximal power are reduced at rates 2- to 5-fold greater than muscle mass, mostly likely from neuromuscular declines [3,4,5,6,7]. Sarcopenia appears to be a loss of muscle fiber size and fiber number, both in slow-twitch muscle fibers and especially in fast-twitch fibers [4,7,8,9,10,11,12,13,14]. Thus, the largest declines in maximal muscle power are generated at fast speeds [6]. This has implications for difficulty in generating rapid muscle power and recovery from an impending fall [3,4,7,15]. Improvements in neuromuscular power production occur most at specific velocities of training, but there appears to be carryover to slower velocities of movement and thus benefits of exercise at high velocity [16,17]. Furthermore, high-speed–high-power training elicited an 11% increase (p < 0.05) in fast-twitch muscle fiber size [17]. Similar responses regarding the specificity of power improvements have been observed in older adults [3,18,19,20,21,22,23,24,25] and during functional tests [26,27]. This indicates that the most effective training might be performed through a large range of velocities with special emphasis on maximal power at high velocities in order to stimulate and hypertrophy fast-twitch muscle fibers.

The author’s research has focused on the physiology of acute exercise and chronic adaptations to exercise training. In recent years, the author has published research on a short daily exercise training program that offsets both the loss of muscle mass and decline in maximal cardiovascular function with age [28,29]. In that these ailments begin at age 30 y and progress in severity with each passing decade [4], a first proactive approach would be to diagnosis the severity of muscle atrophy and impaired function using the method described below for measuring maximal power while cycling with the legs. Presently, there are no objective criteria for diagnosing sarcopenia and maximal leg power might meet the criteria. The second proactive approach to preventing loss of muscle and sarcopenia later in life is to routinely perform exercise throughout adulthood that is most effective and practical for offsetting muscle atrophy. In that atrophy occurs largely due to the shrinkage and loss of fast twitch muscle fibers (FT) [4,12], which are recruited and stimulated by forceful and powerful and fast contractions, the proposed exercise should be short bouts of exercise allowing maximal acceleration or sprinting (i.e.; Sprint Interval Training; SIT) (Figure 1) [30,31]. This review first outlines the major physiological principles supporting ‘all-out’ or maximal acceleration exercise as optimal. Thereafter, it presents a summary of recent publications that provide proof of concept.

Click to view original image

Figure 1 These are typical approximate power outputs of young men and women during exercise that ranges from walking (i.e.; 25 watts) to cycling with maximal power for 4-seconds (i.e.; 1,000 watts) [32]. The main point is that maximal ‘anaerobic’ power production is approximately 500% (5×) higher than maximal ‘aerobic’ power production (i.e.; 200 watts at VO2max). Even ‘high intensity interval training’ (HIIT) only generates approximately 160-240 watts of power, although over 2-10 minutes continuously. ‘Sprint interval training’ (SIT) is performed with maximal effort (‘all-out’) for only 4-30 seconds. The range in maximal power output with SIT is due to methods used to offer resistance when cycling. Much higher power is elicited with ‘Inertial Loading’ compared to a set resistance [33].

2. Safe, Practical and Time Efficient

High intensity exercise, needs to be safe with very little chance of injury. It should allow the person to confidently sprint or accelerate with ‘all-out’ effort. Using free weights for explosive actions presents problems of control if not highly skilled. The safest method is to use leg or arm cycling because all the muscular energy is directed into an accelerating flywheel, which should have a ‘free-wheeling’ mode, allowing the rider to safely disengage and stop. By adjusting the inertial load of the flywheel on the cycle, it is possible to regulate the duration of the sprint which can be extended over several seconds (see below). It is practical to perform SIT with the legs, as this involves the bodies largest muscle mass and because leg fitness dictates ambulation, a key factor for life quality in older adults. SIT can be performed on exercise bikes in either the upright or recumbent position, as the latter is easier to mount for older adults. SIT exercise is routinely performed by children by running as fast as possible and accelerating for a few seconds when playing tag. Unfortunately, most older adults risk muscle or joint injury if attempting to run fast. Flywheel acceleration cycling with a ‘free-wheel’ does not expose a person to eccentric muscle stretching or joint hyperextension and is safe.

Even among older adults, the most commonly cited reason for not exercising is lack of time [34,35,36]. Physical activity guidelines from 2018 [3,37,38,39,40] recommend 150-300 min/week of moderate-intensity physical activity, which may seem daunting. But even lesser amounts at higher intensities can have large benefits [41,42,43]. As discussed below, a workout duration of only 10-minutes, with 1-2 minutes of actual exercise is effective when the power production is high with repeated 4-second accelerations.

2.1 Ethics Statement

All data discussed has been published in journals that have high ethical standards and written Informed Consent to publish such information has been obtained from the individual and approved by the Institutional Review Boards.

3. Maximal Intensity

Undoubtedly, the most important factor for exercise training induced improvements in function is exercise intensity [17,31,42,44]. The premise and effectiveness of SIT is that the exercise is performed as an ‘all-out’ sprint, giving full effort that makes it the maximal voluntary intensity possible [31]. During an ‘all-out’ sprint (cycling or running), a person is recruiting as many motor neurons and muscle fibers as possible. Approximately one-half of our motor neurons and muscle fibers are fast-twitch and these are activated and develop impressive power primarily during sprinting. Unless we compete in powerful competitive sports, we rarely ‘use’ our fast twitch muscle fibers and thus beginning at 30 y, they shrink in size and number and thus we progressively ‘lose’ them (use it or lose it). Participation in high power sports may help serve to offset this loss (e.g.; soccer, tennis, basketball, sprint running, rowing etc.).

Loss of fast-twitch muscle fibers is the major reason for muscle atrophy with age and ultimately sarcopenia, although slow twitch muscle fibers also undergo atrophy with age and disuse [4,7,8,9,10,11,12,13,45,46]. Simply, to proactively prevent muscle atrophy with advancing age, it is necessary to exercise occasionally at or near maximal power for brief periods, ideally throughout adulthood (i.e.; 25-99 years).

Figure 1 demonstrates the cycling powers that are generated by normal young adults when performing various intensities of exercise. The intensity of continuous (e.g.; 5-30 min) aerobic exercise can be expressed in watts and with the corresponding percent of peak oxygen uptake (%VO2max) [46]. An average college student, for example, might reach their aerobic maximum (100% VO2max) when cycling and generating approximately 200 Watts of cycling power. However, when cycling ‘all-out’ for 4-seconds, they can generate an amazing 1,000 Watts of power; the anaerobic maximal power. Maximal anaerobic power is at least five-fold higher (500%) than maximal aerobic power in most people. That indicates that average muscle fiber recruitment is also approximately five times higher when accelerating maximally, than during even the highest intensity of aerobic exercise (VO2max or High Intensity Interval Training). This is a testament to the very high power that fast-twitch muscle fibers can generate when recruited briefly during maximal acceleration.

Another type of interval training that has become popular is high intensity interval training (HIIT), which is high intensity in terms of aerobic stress and lactic acid induced fatigue but is not high intensity in terms of neuromuscular power development (Figure 1) [31]. HIIT is very different in training stimulus from SIT. HIIT is performed for 2-10 minutes and sets the intensity as a percent of aerobic maximum (e.g.; 85-120%) and on average requires an absolute power output of only 200 W (Figure 1). The primary adaptation after a number of weeks of training is an increase in maximal oxygen consumption [31]. Competitive middle-distance runners rely heavily on HIIT and they don’t display much hypertrophy. On the other hand, sprint runners train using bouts lasting only 4-20 s, often focusing on maximal acceleration and speed and they are characterized by substantial hypertrophy. The absolute power generated during SIT is approximately 5× higher than HIIT or the minimal power needed to elicit maximal oxygen consumption (e.g.; 1,000 vs. 200 W) (Figure 1). This magnitude of difference is surprising to some, possibly because popular ergometers and protocols greatly underestimate maximal power [33]. The high power of SIT occurs over a relatively short period of exercise (e.g.; 4-30 seconds) but it can be made more aerobic by performing repetitions with short rest when cycling with maximal power for only 4-seconds [29,47]. This exercise provides high levels of stimulation, simultaneously, for both muscle hypertrophy and cardiovascular function and health [31]. Combining aerobic and resistance training has greater benefits [48] for mobility, especially in the “frail elderly” [49] and this is accomplished with repeated high power accelerations with short rest in between, to stimulate the cardiovascular system.

4. Acceleration

An effective method for stimulating maximal motor unit recruitment is performing an ‘all-out’ cycle acceleration (i.e.; sprint) through the entire range of the torque (force) vs. velocity relationship (Figure 2). This is accomplished by having the rider accelerate as fast as possible, from a dead-stop, up through their maximal velocity (RPM of 150-180). If during the 4-second acceleration the effort is ‘all-out’, the motor unit and muscle fiber recruitment should be maximal, for both slow twitch and fast twitch fibers, as the velocity of contraction progressively increases (i.e.; acceleration). As shown in Figure 2, maximal acceleration through the full-velocity spectrum, elicits three phases. Maximal strength with slow velocity acceleration from 0-60 RPM results in high torque (force) and is characteristic of strength training. Acceleration from 60-130 RPM represents high power which usually is maximal in the range of 110-130 RPM. Finally, continued acceleration from 130-180 RPM (or as high as possible) identifies maximal velocity and high neural activation for coordination. Maximal acceleration and cycling as fast as possible through each of these ranges of velocity is a ‘complete’ method of neuromuscular activation because each range provides a slightly different stimulus of motor unit recruitment and/or firing rate [17]. Cycling through the full range of velocities while exerting maximal effort, seems most effective for FT fiber recruitment and stimulation [19]. Fast-twitch muscle fibers are not recruited in people who limit activity to walking, jogging or short duration aerobic running [50,51,52,53]. Thus, these low power activities may not be sufficient to prevent the loss of fast-twitch muscle fibers with aging.

Click to view original image

Figure 2 When performing a maximal cycling acceleration lasting 4-seconds, the person (a young male or female) accelerates as fast as possible by pushing on the pedals as forcefully as possible as the velocity of the flywheel increases. In accordance with muscle mechanics, the force (torque) generating ability of the myofilaments declines as energy is directed to increasing velocity and power increases (torque × velocity). There is a velocity (e.g.; 110-130 RPM of cycling) of myofilament shortening that is most efficient at capturing the energy from ATP hydrolysis and thus generates the maximal power. Therefore, there are 3 general phases of a maximal acceleration. The ‘strength phase’ in accelerating from 0 to 60 RPM feels hardest as high forces are needed to get the flywheel moving. As velocity increases from 60 to 130 RPM, power increases and ‘maximal power’ is reached between 110-130 RPM depending on the individuals muscle composition of slow and fast-twitch fibers [54]. At velocities above 130 RPM, the ‘speed’ range, power declines as torque is lowered to the point of no acceleration and thus no power. Training in the ‘speed’ range feels easy because of the feedback from low force, but effort is still high and neural recruitment of fast-twitch motor neurons is probably still high [17].

5. Maximal Power

Power is simply the product of torque (force) and velocity. As the velocity of muscle contraction increases the sliding myofilaments are naturally less able to generate force. With force declining as velocity increases, the maximal power is reached at a specific velocity (e.g.; 110-130 RPM) (Figure 2) that has optimal efficiency for the myofilaments to capture ATP energy and thus generate maximal power. Power can be very accurately calculated during a sprint by monitoring the velocity and thus the acceleration of the ergometer flywheel, of known inertial load (i.e.; moment of inertial and gearing). Power is torque × velocity. Torque (force) is defined as moment of inertial × acceleration. Thus, instantaneous power can be calculated as the inertial load × acceleration × velocity. Maximal power can thus be identified as in Figure 2. It is largely a function of acceleration with an added contribution of high velocity. It has been shown in clinical trials of older adults that exercise at higher speeds and power compared to training at slower speeds for strength is more effective for reducing the risk of falls, a serious threat for older adults [7,21].

6. Inertial Load

An extremely precise method of applying a constant and natural resistive load to the flywheel during a cycle sprint is to simply calculate inertial load from the moment of inertial of the flywheel and cycle gearing. Inertial is a force described by Newton that resists the acceleration or deceleration of a moving object. As with gravity, we don’t understand what causes an inertial force, yet we have learned how to use it. Functionally, we use inertia as the natural constant force that resists acceleration of the flywheel throughout the sprint. Almost all cycle ergometers add resistance to the flywheel using crude friction or magnets, that are imprecise, difficult to calibrate, variable and costly. If maximal sprint power from acceleration measurements were attempted on these devices, they would need to account for the power to overcome inertia [55]. Additionally, it is impossible to know what resistive load to apply during the sprint because people differ tremendously in thigh muscle mass [33,56]. Isokinetic cycles that control velocity have less variability than those applying a set resistance, but usually require several trials at a range of velocities [55,57]. In essence, ‘Inertial Loading’ is not just more direct and precise, its simpler and it allows maximal power can be identified with just one acceleration as compared with methods that require several sprints against various resistances and velocities.

7. Length of Sprint

With sprint cycling, we have seen that the same approximate maximal power values can be achieved with accelerations (from 0-180 RPM) that take 1 to 4 seconds, varied by altering the inertial loads. The energy source for these durations are chemicals stored in muscle fibers in the form of ATP and Phospho-Creatine (PCr). Although they can provide energy at very high rates, their stores become depleted after several seconds of sprinting. The goal with repeated sprints is to sprint long enough for PCr to power the exercise but not so much that it can’t be largely resynthesized by oxidative metabolism during the short recovery periods. This work-rest ratio elicits a reasonable VO2 response and thus cardiovascular stimulation, a secondary goal of the workouts. Accelerations extending to 6 seconds or longer, might cause fatigue by over stimulating glycogenolysis and acid production when repeated sprints are performed [58]. Four second sprints seemed the most accommodating duration because it allowed time to be spent in each of the three domains of strength, power and speed. Furthermore, it is not fatiguing and doesn’t raise blood lactate levels to very high levels (i.e.; <6.5 mM) after the most strenuous workout of 30 sprints with 15 seconds recovery (Figure 3) [29].

Click to view original image

Figure 3 Progressively shorter rest periods (45, 30 or 15 seconds) between ‘all-out’ 4-second accelerations (30×) results in a graded increase in oxygen consumption (VO2), with all trials reaching a pseudo-steady state with fluctuations of ±5% VO2 in synchrony with the 4-second accelerations. All three trials elicited between 49-72% VO2peak and corresponding levels of % maximal heart rate (75-86% HRmax). These values are in the prescriptive range for promoting aerobic adaptations. Reproduced with permission [29].

8. Recovery Duration for Cardiovascular Simulation

As mentioned, the decision behind a 4-second sprint duration was to not lower PCr too much or increase glycogenolysis too much to cause fatigue with repeated bouts. The goal is to have a reasonable recovery of muscle metabolism (measured via NIRS) via a relatively high O2 delivery, high VO2 and high heart rate (HR), throughout the 10-minute workout [29]. As shown in Figure 3, recovery durations of 45, 30 and 15 seconds over 30 sprints resulted in VO2 responses that elicited 49, 56 and 72% VO2peak, respectively. Similarly, the HR responses were 75, 80 and 86% of maximal HR. Given that these cardiovascular responses were nicely graded between different recovery durations and that they all were in the recommended prescriptive zone for cardiovascular adaptations, it appears that repeated 4-second sprint training is a reliable and practical method of cardiovascular stimulation that is graded and increased by reducing the rest period. It is also an effective method for raising VO2peak after 8 weeks of training, along with improving arterial elasticity in older adults.

9. 10-Minute Duration and Training Progression

Of course, the recovery duration between sprints will dictate the number of sprints that can be completed in a 10-minute period with 12, 18 and 30 sprints possible when taking 45, 30, and 15-seconds of recovery, respectively. Only 1-2 minutes of exercise are completed in a 10-minute period. From a practical perspective, a training session lasting only 10-minutes does not elicit a heavy sweating response and thus the exercise can be performed in street clothes. Shorter rest is accompanied by more frequent sprints that raise the level of cardiovascular stimulation. Therefore, a progression of the training stimuli and subsequent further adaptations are achieved by reducing the rest period every few weeks and thus increasing the cardiovascular stress and total number of sprints.

10. The NASA Experiment

In addition to aging and sarcopenia, significant muscle loss is experienced with prolonged bed rest as well as prolonged exposure to the microgravity during space flight. Clearly, the muscle atrophy from bed rest and microgravity are due to disuse (‘use it or lose it’), and the atrophy with aging appears to have a large component of disuse that might be countered with exercise, especially if it is intense [28]. NASA uses the complete bedrest model to induce muscle atrophy over a 70-day period and in their bedrest control group, receiving no exercise training, they typically report a 15-20% reduction in the area of the vastus lateralis [46]. However, in a recent publication [46], NASA scientists, in an effort to accurately measure maximal power throughout the 70 days in the bedrest control group, employed our inertial load ergometer and the 4-second acceleration exercise on 9 occasions (every ~8 days) and had subjects perform 6 sprints of 4-seconds each (total only 24 seconds every 8 days). They also measured aerobic power on 4 occasions (every ~17 days). They were surprised to find that the amount of whole muscle atrophy of the bedrest-control group was only one-half of what has been previously shown. More surprising was their observation, using sophisticated single fiber techniques, that the fast-twitch muscle fibers (Type II) of the bedrest control group displayed no loss in fiber size or maximal power. Furthermore, the loss of slow-twitch fiber size and power was less than previously observed. Bedrest, like aging, normally results in a large loss of whole muscle size as well as a shrinkage of fast-twitch muscle size [46]. Apparently, the small amount of acceleration exercise encountered by the testing to assess maximal muscle power and aerobic power was enough to totally prevent atrophy of the fast-twitch fibers. Although we can’t discount the contribution of the less frequent aerobic power measures, a potent stimulation of fast-twitch muscle fibers by the more frequent 4-second maximal acceleration exercise agrees with the hypotheses discussed above. These observations provide strong support for the use of 4-second acceleration exercise to offset fast-twitch fiber atrophy and weakness.

Surprised by the observation that only 24-seconds (4-seconds × 6) of maximal acceleration exercise might produce a powerful stimulus that maintains fast-twitch fiber size and power, these NASA investigators measured the molecular responses to a single session (4-seconds × 6) of maximal acceleration cycling [59]. They targeted muscle gene responses (i.e.; mRNA) both in mixed muscle homogenates as well as in isolated single fast-twitch and slow-twitch muscle fibers. The brief cycling was effective at activating genes that signal muscle growth (e.g.; IκBa, myogenin, MuRF-1, RRAD, Fn14) in the whole mixed fiber muscle. Furthermore, it was more effective at activating genes and mRNA in the fast-twitch than the slow-twitch muscle fibers [59]. These molecular findings agree with this group’s prior observation that very brief bouts of maximal acceleration cycling seem to serve as a potent countermeasure to muscle atrophy of fast-twitch fibers during prolonged bed rest. Again, given that the muscle atrophy of aging is also due largely to reductions in fast-twitch muscle fiber size, it seemed likely to us that healthy older adults might respond well to 8 weeks of cycle training based on repeated 4-second bouts of maximal acceleration.

11. 4-Second Acceleration Training

We recruited untrained men and women between the ages of 50-69 years (n = 29). They trained 3 times per week for 8 weeks and during each session they performed 12-30 maximal accelerations lasting 4-seconds and rested 26-45 seconds between accelerations [28]. The training stimulus progressed by taking shorter rest and performing more repetitions. In another study [32], we recruited 11 young (21 y) untrained men and women who performed similar training as described above for the older adults. In both studies, the length of the training sessions decreased from ~15 minutes to 10 minutes.

The results from training for both groups indicate the following [28,32]. Most importantly, the older adults showed a significant increase in lean thigh volume measured with MRI. This measure was not made in the young adults. Maximal muscle power increased 13-17% (p < 0.05) in both groups, which probably explained the increases in the functional tasks of living in older adults and vertical jump in the young adults. Furthermore, both groups displayed significant increases in maximal oxygen consumption (9.8-13.2%; p < 0.05) while the older adults also displayed significant improvements in arterial elasticity (not measured in young adults). Surprisingly, blood volume increased 7.5% in the young adults (not measured in older adults).

Clearly, both young and old adults displayed robust improvements after 8 weeks from training sessions that lasted 10-15 minutes and involved only 1-2 minutes of exercise. Significant increases were found both in muscle size and maximal power as well as in the function and health of the cardiovascular system. These observations demonstrate that maximal acceleration cycling or SIT exercise can simultaneously stimulate muscle hypertrophy and improvements in cardiovascular function.

12. Summary

Proactive treatment for the loss of muscle mass beginning after 30 y and progressing throughout adulthood, requires two proactive approaches. The first is to diagnose the loss of function using sensitive, safe and valid cycling power tests. The second is to prevent or offset muscle atrophy, especially of the fast-twitch muscle fibers, through 4-second acceleration training from cycling as fast as possible against an inertial load. With this, improved power and endurance are gained from the training sessions, that cause little fatigue and require only 10 minutes.

Acknowledgments

The graduate students of Dr. Coyle at the University of Texas are recognized for their contributions over the past two decades.

Author Contributions

Dr. Coyle was the sole contributor to this article with recognition and citation of research collaborators.

Funding

This review article was unfunded.

Competing Interests

Dr. Coyle owns Sports Texas Inc., a company that has made and sold the Power Cycle discussed in this article until 2021. Future commercial plans are undecided.

References

  1. Cruz-Jentoft AJ, Landi F, Schneider SM, Zúñiga C, Arai H, Boirie Y, et al. Prevalence of and interventions for sarcopenia in ageing adults: A systematic review. Report of the International Sarcopenia Initiative (EWGSOP and IWGS). Age Ageing. 2014; 43: 748-759. [CrossRef] [Google scholar] [PubMed]
  2. Cruz-Jentoft AJ, Bahat G, Bauer J, Boirie Y, Bruyère O, Cederholm T, et al. Sarcopenia: Revised European consensus on definition and diagnosis. Age Ageing. 2019; 48: 16-31. [CrossRef] [Google scholar] [PubMed]
  3. Aversa Z, Zhang X, Fielding RA, Lanza I, LeBrasseur NK. The clinical impact and biological mechanisms of skeletal muscle aging. Bone. 2019; 127: 26-36. [CrossRef] [Google scholar] [PubMed]
  4. Larsson L, Degens H, Li M, Salviati L, Lee YI, Thompson W, et al. Sarcopenia: Aging-related loss of muscle mass and function. Physiol Rev. 2019; 99: 427-511. [CrossRef] [Google scholar] [PubMed]
  5. Young A, Skelton D. Applied physiology of strength and power in old age. Int J Sports Med. 1994; 15: 149-151. [CrossRef] [Google scholar] [PubMed]
  6. Petrella JK, Kim JS, Tuggle SC, Hall SR, Bamman MM. Age differences in knee extension power, contractile velocity, and fatigability. J Appl Physiol. 2005; 98: 211-220. [CrossRef] [Google scholar] [PubMed]
  7. Reid KF, Fielding RA. Skeletal muscle power: A critical determinant of physical functioning in older adults. Exerc Sport Sci Rev. 2012; 40: 4-12. [CrossRef] [Google scholar] [PubMed]
  8. Tomonaga M. Histochemical and ultrastructural changes in senile human skeletal muscle. J Am Geriatr Soc. 1977; 25: 125-131. [CrossRef] [Google scholar] [PubMed]
  9. Larsson L, Sjödin B, Karlsson J. Histochemical and biochemical changes in human skeletal muscle with age in sedentary males, age 22-65 years. Acta Physiol Scand. 1978; 103: 31-39. [CrossRef] [Google scholar] [PubMed]
  10. Lexell J, Henriksson‐Larsén K, Winblad B, Sjöström M. Distribution of different fiber types in human skeletal muscles: Effects of aging studied in whole muscle cross sections. Muscle Nerve. 1983; 6: 588-595. [CrossRef] [Google scholar] [PubMed]
  11. Lexell J, Taylor CC, Sjöström M. What is the cause of the ageing atrophy?: Total number, size and proportion of different fiber types studied in whole vastus lateralis muscle from 15-to 83-year-old men. J Neurol Sci. 1988; 84: 275-294. [CrossRef] [Google scholar] [PubMed]
  12. Larsson L, Li X, Frontera W. Effects of aging on shortening velocity and myosin isoform composition in single human skeletal muscle cells. Am J Physiol Cell Physiol. 1997; 272: C638-C649. [CrossRef] [Google scholar] [PubMed]
  13. Cristea A, Qaisar R, Edlund PK, Lindblad J, Bengtsson E, Larsson L. Effects of aging and gender on the spatial organization of nuclei in single human skeletal muscle cells. Aging Cell. 2010; 9: 685-697. [CrossRef] [Google scholar] [PubMed]
  14. Brocca L, McPhee JS, Longa E, Canepari M, Seynnes O, De Vito G, et al. Structure and function of human muscle fibres and muscle proteome in physically active older men. J Physiol. 2017; 595: 4823-4844. [CrossRef] [Google scholar] [PubMed]
  15. Larsson L, Grimby G, Karlsson J. Muscle strength and speed of movement in relation to age and muscle morphology. J Appl Physiol. 1979; 46: 451-456. [CrossRef] [Google scholar] [PubMed]
  16. Caiozzo VJ, Perrine JJ, Edgerton VR. Training-induced alterations of the in vivo force-velocity relationship of human muscle. J Appl Physiol. 1981; 51: 750-754. [CrossRef] [Google scholar] [PubMed]
  17. Coyle EF, Feiring D, Rotkis T, Cote III R, Roby F, Lee W, et al. Specificity of power improvements through slow and fast isokinetic training. J Appl Physiol. 1981; 51: 1437-1442. [CrossRef] [Google scholar] [PubMed]
  18. Earles DR, Judge JO, Gunnarsson OT. Velocity training induces power-specific adaptations in highly functioning older adults. Arch Phys Med Rehabil. 2001; 82: 872-878. [CrossRef] [Google scholar] [PubMed]
  19. LeBrasseur NK, Cuoco A, Bean J, Mizer K, Fielding RA. Impact of high velocity power training on strength & power in older women. Med Sci Sports Exerc. 2001; 33: S344. [CrossRef] [Google scholar]
  20. Fielding RA, LeBrasseur NK, Cuoco A, Bean J, Mizer K, Singh MAF. High‐velocity resistance training increases skeletal muscle peak power in older women. J Am Geriatr Soc. 2002; 50: 655-662. [CrossRef] [Google scholar] [PubMed]
  21. Reid KF, Martin KI, Doros G, Clark DJ, Hau C, Patten C, et al. Comparative effects of light or heavy resistance power training for improving lower extremity power and physical performance in mobility-limited older adults. J Gerontol A Biomed Sci Med Sci. 2015; 70: 374-380. [CrossRef] [Google scholar] [PubMed]
  22. Balachandran AT, Gandia K, Jacobs KA, Streiner DL, Eltoukhy M, Signorile JF. Power training using pneumatic machines vs. plate-loaded machines to improve muscle power in older adults. Exp Gerontol. 2017; 98: 134-142. [CrossRef] [Google scholar] [PubMed]
  23. Beijersbergen CM, Granacher U, Gaebler M, Devita P, Hortobágyi T. Power training-induced increases in muscle activation during gait in old adults. Med Sci Sports Exerc. 2017; 49: 2198-2205. [CrossRef] [Google scholar] [PubMed]
  24. Inacio M, Creath R, Rogers MW. Low-dose hip abductor-adductor power training improves neuromechanical weight-transfer control during lateral balance recovery in older adults. Clin Biomech. 2018; 60: 127-133. [CrossRef] [Google scholar] [PubMed]
  25. Katsoulis K, Stathokostas L, Amara CE. The effects of high-versus low-intensity power training on muscle power outcomes in healthy, older adults: A systematic review. J Aging Phys Act. 2019; 27: 422-439. [CrossRef] [Google scholar] [PubMed]
  26. Orr R, De Vos NJ, Singh NA, Ross DA, Stavrinos TM, Fiatarone-Singh MA. Power training improves balance in healthy older adults. J Gerontol A Biol Sci Med Sci. 2006; 61: 78-85. [CrossRef] [Google scholar] [PubMed]
  27. Byrne C, Faure C, Keene DJ, Lamb SE. Ageing, muscle power and physical function: A systematic review and implications for pragmatic training interventions. Sports Med. 2016; 46: 1311-1332. [CrossRef] [Google scholar] [PubMed]
  28. Allen JR, Satiroglu R, Fico B, Tanaka H, Vardarli E, Luci JJ, et al. Inertial load power cycling training increases muscle mass and aerobic power in older adults. Med Sci Sports Exerc. 2021; 53: 1188-1193. [CrossRef] [Google scholar] [PubMed]
  29. Vardarli E, Satiroglu R, Allen JR, Bjellquist-Ledger R, Burton HM, Coyle EF. Physiological responses to maximal 4 s sprint interval cycling using inertial loading: The influence of inter-sprint recovery duration. Eur J Appl Physiol. 2021; 121: 2295-2304. [CrossRef] [Google scholar] [PubMed]
  30. Gava P, Kern H, Carraro U. Age-associated power decline from running, jumping, and throwing male masters world records. Exp Aging Res. 2015; 41: 115-135. [CrossRef] [Google scholar] [PubMed]
  31. Boullosa D, Dragutinovic B, Feuerbacher JF, Benítez‐Flores S, Coyle EF, Schumann M. Effects of short sprint interval training on aerobic and anaerobic indices: A systematic review and meta‐analysis. Scand J Med Sci Sports. 2022; 32: 810-820. [CrossRef] [Google scholar] [PubMed]
  32. Satiroglu R, Lalande S, Hong S, Nagel MJ, Coyle EF. 4-s inertial load sprint training raises maximal anaerobic power, peak oxygen consumption and blood volume. Med Sci Sports Exerc. 2021; 53: 2536-2542. [CrossRef] [Google scholar] [PubMed]
  33. Coso JD, Mora-Rodríguez R. Validity of cycling peak power as measured by a short-sprint test versus the Wingate anaerobic test. Appl Physiol Nutr Metab. 2006; 31: 186-189. [CrossRef] [Google scholar] [PubMed]
  34. Stutts WC. Physical activity determinants in adults: Perceived benefits, barriers, and self efficacy. AAOHN J. 2002; 50: 499-507. [CrossRef] [Google scholar]
  35. Trost SG, Owen N, Bauman AE, Sallis JF, Brown W. Correlates of adults’ participation in physical activity: Review and update. Med Sci Sports Exerc. 2002; 34: 1996-2001. [CrossRef] [Google scholar] [PubMed]
  36. Gillen JB, Gibala MJ. Is high-intensity interval training a time-efficient exercise strategy to improve health and fitness? Appl Physiol Nutr Metab. 2014; 39: 409-412. [CrossRef] [Google scholar] [PubMed]
  37. Troiano RP, Berrigan D. Physical activity in the United States measured by accelerometer: Comment-response. Med Sci Sports Exerc. 2008; 40: 1189. [CrossRef] [Google scholar]
  38. Troiano RP, Berrigan D, Dodd KW, Masse LC, Tilert T, McDowell M. Physical activity in the United States measured by accelerometer. Med Sci Sports Exerc. 2008; 40: 181-188. [CrossRef] [Google scholar] [PubMed]
  39. Tudor-Locke C, Hart TL, Washington TL. Expected values for pedometer-determined physical activity in older populations. Int J Behav Nutr Phys Act. 2009; 6: 59. [CrossRef] [Google scholar] [PubMed]
  40. Booth FW, Roberts CK, Thyfault JP, Ruegsegger GN, Toedebusch RG. Role of inactivity in chronic diseases: Evolutionary insight and pathophysiological mechanisms. Physiol Rev. 2017; 97: 1351-1402. [CrossRef] [Google scholar] [PubMed]
  41. Rodas G, Ventura JL, Cadefau JA, Cussó R, Parra J. A short training programme for the rapid improvement of both aerobic and anaerobic metabolism. Eur J Appl Physiol. 2000; 82: 480-486. [CrossRef] [Google scholar] [PubMed]
  42. Coyle EF. Very intense exercise-training is extremely potent and time efficient: A reminder. J Appl Physiol. 2005; 98: 1983-1984. [CrossRef] [Google scholar] [PubMed]
  43. Powell KE, King AC, Buchner DM, Campbell WW, DiPietro L, Erickson KI, et al. The scientific foundation for the physical activity guidelines for Americans. J Phys Act Health. 2018; 16: 1-11. [CrossRef] [Google scholar] [PubMed]
  44. Dudley GA, Abraham WM, Terjung RL. Influence of exercise intensity and duration on biochemical adaptations in skeletal muscle. J Appl Physiol. 1982; 53: 844-850. [CrossRef] [Google scholar] [PubMed]
  45. Evans WJ, Lexell J. Human aging, muscle mass, and fiber type composition. J Gerontol A Biol Sci Med Sci. 1995; 50: 11-16. [CrossRef] [Google scholar] [PubMed]
  46. Trappe TA, Minchev K, Perkins RK, Lavin KM, Jemiolo B, Ratchford SM, et al. NASA SPRINT exercise program efficacy for vastus lateralis and soleus skeletal muscle health during 70 days of simulated microgravity. J Appl Physiol. 2024; 136: 1015-1039. [CrossRef] [Google scholar] [PubMed]
  47. Van Baak M, Mooij J. Effect of glucose infusion on endurance performance after beta-adrenoceptor blocker administration. J Appl Physiol. 1994; 77: 641-646. [CrossRef] [Google scholar] [PubMed]
  48. Mcleod JC, Stokes T, Phillips SM. Resistance exercise training as a primary countermeasure to age-related chronic disease. Front Physiol. 2019; 10: 645. [CrossRef] [Google scholar] [PubMed]
  49. Theou O, Stathokostas L, Roland KP, Jakobi JM, Patterson C, Vandervoort AA, et al. The effectiveness of exercise interventions for the management of frailty: A systematic review. J Aging Res. 2011; 2011: 569194. [CrossRef] [Google scholar] [PubMed]
  50. Gollnick P, Piehl K, Saubert 4th C, Armstrong R, Saltin B. Diet, exercise, and glycogen changes in human muscle fibers. J Appl Physiol. 1972; 33: 421-425. [CrossRef] [Google scholar] [PubMed]
  51. Gollnick PD, Armstrong R, Saubert Iv C, Sembrowich W, Shepherd R, Saltin B. Glycogen depletion patterns in human skeletal muscle fibers during prolonged work. Pflugers Arch. 1973; 344: 1-12. [CrossRef] [Google scholar] [PubMed]
  52. Piehl K, Gollnick P, Saltin B. Selective glycogen depletion in muscle-fibers during prolonged exercise. J Physiol. 1974; 241: 45-57. [CrossRef] [Google scholar] [PubMed]
  53. Gollnick P, Piehl K, Saltin B. Selective glycogen depletion pattern in human muscle fibres after exercise of varying intensity and at varying pedalling rates. J Physiol. 1974; 241: 45-57. [CrossRef] [Google scholar] [PubMed]
  54. Coyle EF, Costill DL, Lesmes GR. Leg extension power and muscle fiber composition. Med Sci Sports. 1979; 11: 12-15. [Google scholar]
  55. Lakomy H. Measurement of work and power output using friction-loaded cycle ergometers. Ergonomics. 1986; 29: 509-517. [CrossRef] [Google scholar] [PubMed]
  56. Martin J, Farrar R, Wagner B, Spirduso W. Maximal power across the lifespan. J Gerontol A Biol Sci Med Sci. 2000; 55: M311-M316. [CrossRef] [Google scholar] [PubMed]
  57. Lakomy H. An ergometer for measuring the power generated during sprinting. J Physiol. 1984; 354: 33P. [Google scholar]
  58. Bogdanis G, Nevill M, Lakomy H, Boobis L. Power output and muscle metabolism during and following recovery from 10 and 20 s of maximal sprint exercise in humans. Acta Physiol Scand. 1998; 163: 261-272. [CrossRef] [Google scholar] [PubMed]
  59. Voss AC, Chambers TL, Gries KJ, Jemiolo B, Raue U, Minchev K, et al. Exercise microdosing for skeletal muscle health applications to spaceflight. J Appl Physiol. 2024; 136: 1040-1052. [CrossRef] [Google scholar] [PubMed]
Newsletter
Download PDF Download Full-Text XML Download Citation
0 0
Newsletter  

TOP