Soccer vs. Running in Type 2 Diabetes: A Muscle Signal

Soccer and running produced different muscle-gene signals in a small trial of older adults with type 2 diabetes. Soccer lowered two genes linked to muscle protein breakdown; running raised a gene linked to exercise signaling. Yet after 12 weeks, the study did not show that either activity built more muscle, improved strength, or beat diet alone for blood sugar control.

That distinction matters. A muscle biopsy can detect biological changes long before a scale, strength test, or DXA scan does. It can also detect a short-lived response that never becomes a meaningful health outcome. This trial offers an interesting molecular clue, not a reason for an older adult with type 2 diabetes to trade running shoes for cleats.

Three groups, one calorie deficit

The randomized controlled trial enrolled 39 adults with type 2 diabetes, average age 60 years, with an average BMI of 33.5 kg/m². Participants completed 12 weeks of one of three programs: recreational soccer plus an approximately 500-kcal-per-day calorie deficit, continuous running plus the same calorie deficit, or calorie restriction alone. Researchers took biopsies from the vastus lateralis, a large thigh muscle, before and after the intervention.

The design had a real advantage over many exercise studies: the diet-only group tested whether exercise added a signal beyond weight-loss dieting. All three groups lost about 4 kg of fat mass and improved HbA1c to a similar extent. The trial therefore gives no evidence that soccer or running produced superior fat loss or glycemic control during those 12 weeks.

The differences appeared in messenger RNA, the instructions cells use to make proteins. In the soccer-plus-diet group, ATROGIN-1 expression fell from 1.084 to 0.754 relative-expression units, about 30%, and MuRF-1 fell from 1.175 to 0.693, about 41%; both changes were reported as statistically significant at p<0.05. In the running-plus-diet group, IL-15 expression rose from 1.056 to 1.308, about 24%, also with p<0.05. The diet-only group had no statistically significant change in these three markers.

Why those genes drew attention

ATROGIN-1 and MuRF-1 encode ubiquitin E3 ligases, components of the ubiquitin-proteasome system that tags proteins for degradation. Higher expression commonly accompanies muscle-wasting states. In mouse research, increased atrogin-1 and MuRF-1 accompanied lower muscle mass, grip strength, and muscle-fiber size, although animal findings cannot establish the same outcome in people. Lu et al. provide that mechanistic context, not proof that a 41% reduction in MuRF-1 mRNA preserves human muscle.

IL-15 is a myokine: a signaling molecule associated with skeletal muscle and exercise-related metabolic and inflammatory adaptation. A 2026 meta-analytic compendium of exercise studies in older adults found improvements across many metabolic and inflammatory outcomes with training. But the soccer-running trial measured IL-15 mRNA in one muscle sample. It did not measure circulating IL-15, IL-15 protein, downstream signaling, or a clinical effect caused by IL-15.

The pattern is biologically plausible. Recreational soccer includes accelerations, decelerations, changes of direction, and intermittent high-intensity work. Continuous running provides a steadier aerobic stimulus. Those demands could produce different transcriptional responses in muscle. Plausible is the correct word: the study cannot tell whether the observed gene changes came from exercise mode itself, variation in food intake, individual biology, or chance patterns in a small sample.

The missing outcome is function

Muscle mRNA is a surrogate endpoint. The outcomes people actually need include lean mass, strength, walking capacity, chair-rise performance, falls, and independent function. This study did not report handgrip strength, gait speed, a six-minute walk test, repeated chair stands, or standard EWGSOP2 sarcopenia measures. Although DXA data were collected, the abstract did not report lean-mass results by exercise group.

That leaves a large gap between lower expression of two catabolic markers and lower risk of sarcopenia. Protein synthesis and protein breakdown determine muscle tissue over time; mRNA alone does not measure either process. A 2026 trial in older women found that resistance exercise plus essential amino acids changed an anabolic-to-catabolic marker ratio alongside improved muscle fitness. Its intervention, population, and outcomes differ substantially from 12 weeks of aerobic exercise in adults with type 2 diabetes, but it illustrates the standard this soccer-running study did not meet: pair molecular findings with measurable function.

The trial was also small: roughly 13 people per group. The reported post-intervention ATROGIN-1 standard deviation in the soccer group, 1.14, exceeded the mean value of 0.754. That spread makes the group estimate uncertain and raises questions about distributional assumptions. The reported p-values do not solve that problem; individual data, confidence intervals, and the full statistical analysis would matter greatly here.

Diet is a competing explanation, not background scenery

Each group followed a substantial calorie deficit, and each achieved similar fat loss and HbA1c improvement. Calorie restriction can alter whole-body energy balance and metabolic signaling without exercise. The diet-only arm did not show significant changes in the three measured genes, which is compatible with an exercise-related signal, but it does not establish that soccer itself caused the soccer-group changes.

Diet composition adds another uncertainty. Protein intake can influence inflammatory and catabolic biology in older adults. A 2025 systematic review and meta-analysis of randomized trials examined exercise and protein intake in relation to inflammaging, supporting the idea that both exposures matter. Without evidence that protein and other macronutrients were equivalent across the three groups, exercise modality remains an incomplete explanation.

Nor does the broader literature settle a soccer-versus-running contest. A 12-week study of high-intensity interval training in obese older adults found preserved skeletal muscle mass and lower adiposity, but it had no matched continuous-running group and did not measure ATROGIN-1 or MuRF-1. Marcangeli et al. therefore support the plausibility of intermittent exercise, not the superiority of soccer.

What current evidence supports

For older adults with type 2 diabetes, aerobic activity has established benefits for metabolic health, and exercise training can improve cardiac autonomic measures. A systematic review of exercise training in type 2 diabetes found improvements in heart-rate-variability measures, though protocols varied. The more consistent evidence for body composition and physical function comes from programs that combine aerobic and resistance training.

A 2025 meta-analysis of adults with type 2 diabetes and overweight or obesity evaluated concurrent aerobic and resistance training and found benefits for body composition, lipid metabolism, and physical function. A 2024 meta-analysis in middle-aged and older adults with type 2 diabetes likewise evaluated combined aerobic-resistance programs and reported improvements in metabolic health and physical function. These findings cannot tell us whether soccer beats running, but they do support resistance loading as the better-supported addition when muscle preservation and function are the goals.

The trial found a molecular difference between soccer and running. It did not find a difference in muscle mass, strength, function, fat loss, or HbA1c.

The practical verdict

Choose soccer if you enjoy it, can participate safely, and will keep showing up. Choose running if it suits your joints, fitness, and preferences. The study suggests that these activities may send different signals to thigh muscle, but it does not show that one protects muscle better in older adults with type 2 diabetes.

If muscle preservation is the priority during fat loss, the evidence points to a more established plan: regular aerobic activity, progressive resistance training, and adequate dietary protein tailored with a clinician or dietitian when kidney disease or other medical issues are present. The soccer result is hypothesis-grade evidence: 12 weeks, about 13 participants per group, and mRNA outcomes without a confirmed functional result. It earns follow-up research, not a clinical prescription.