Why Being Fit Can Offset Being Overweight
In grad school, I researched a group of unicorns that we called fat but fit.
These people met the clinical criteria to be classified as overweight but were regular exercisers and could hit the VO2 max numbers of a trained person.
The study explored how exercise mitigates the health risks of being overweight. Research consistently shows that regular physical activity lowers disease risk, often making active, overweight individuals healthier than sedentary individuals at a normal weight.
In fact, fitness level appears to be a stronger predictor of health than body weight alone, and increased physical activity is shown to enhance key health markers, such as metabolic function and cardiovascular health, even in the absence of weight loss.
My research focused on how exercise lowers systemic inflammation, which certainly remains compelling, but as of late, it seems that the slam dunk for exercise is its impact on the machinery for how cells make energy—tiny cell powerhouses called mitochondria.
Now, I'll highlight the big take-home point first because some of you might no longer care to read any longer. But I've seen a few things lately that belittle exercise since it's largely ineffective for weight loss.
I agree that diet is the cornerstone for dropping pounds, especially when simply looking at the calorie deficit equation.
But we cannot overlook the role that aerobic fitness (long, slow aerobic stuff) has on living a long life and fighting chronic disease, especially for its role in keeping our fuel systems running efficiently, which could also be better for weight loss.
Mitochondria and Disease
As you may remember from 6th-grade biology, mitochondria are not a new discovery.
However, what has changed is our understanding of how the mitochondria regulate fuel usage and the importance of lactate as a fuel source.
If you're interested in this stuff, a recent review by Dr. Iñigo San-Millán highlights how dysfunction in the programming of mitochondria disrupts a number of pathways in how the body functions.
The following are some of the ways a breakdown in your mitochondria contributes to conditions like Type 2 diabetes, cardiovascular disease, dementia, cancer, and what seems like all the plagues of old age.
- Metabolic Inflexibility - This refers to the body's ability to efficiently switch between using carbohydrates and fats for energy, depending on what's available and needed. A person with good metabolic flexibility can easily burn fat at rest and shift to using carbs during high-intensity activities.
- Increases Oxidative Stress - As the body burns fuel, it generates an exhaust called reactive oxygen species (ROS), which are unstable molecules that can damage cells. While some ROS play essential roles in cell signaling and immune defense, excessive ROS leads to cellular damage, inflammation, and accelerated aging.
- Impairs Cellular Repair Mechanisms - When mitochondria are not functioning properly, cells struggle to repair themselves effectively. This can lead to slower recovery from injuries, reduced ability to replace damaged cells, and an overall decline in tissue health. Over time, this contributes to aging, chronic inflammation, and increased susceptibility to diseases.
The Changing Tune on Lactate
A growing body of research has also revolutionized our understanding of lactate as cell fuel.
Once thought of as a waste product that inhibited performance, it is now recognized as a crucial fuel source for mitochondria. During exercise, lactate is shuttled to cells with high energy demands, where it is efficiently converted into energy.
This means that well-trained individuals tolerate lactate better and use it more effectively to power performance and recovery. Another interesting point about lactate is that it inhibits fat utilization by the cell.
The below graph from the review paper shows that improves our ability to use lactate as fuel lowers lactate levels, improving our ability to use fat as the preferred energy source.
Exercise is the Best "Medicine"
Exercise is one of the most potent tools for maintaining and improving mitochondrial function.
It stimulates mitochondrial biogenesis—the process of forming new mitochondria—enhancing overall cellular energy capacity. Exercise also increases mitochondrial efficiency, allowing cells to produce more energy with less oxidative stress. This boosts athletic performance and is vital to metabolic health and disease prevention.
It costs nothing and has few side effects—the perfect medical intervention.
However, the current recommendations of: "At least 150 minutes per week of moderate-intensity aerobic activity or 75 minutes per week of vigorous aerobic activity, or a combination of both, preferably spread throughout the week" appear to be on the low end of what we might need.
Studies show that 12 weeks of endurance training (5 days/week) can double mitochondrial enzyme levels and increase total mitochondria by 60%. Similarly, 10 weeks of daily endurance training can boost mitochondrial concentration in skeletal muscle by about 30%
Based on other information I've pulled from Dr. San-Millán (here is a great podcast with him), we should ideally aim for 90 minutes of Zone 2 exercise about 4x per week, which is a comfortable talking pace.
Obviously, that might take some building up, and anything is better than nothing.
Originally published as Movement #253
