What if the player who goes down on day three of two-a-days isn’t undertrained — but living in a sympathetic state nobody thought to measure?

By Dr. Robert L. Janda, MA, DC

September 14, 2016 · Issue 15 · Newport Beach, California

A study published last month in the Journal of Athletic Training tracked heat-related injuries across a season of pre-season football practice at the University of Georgia. The numbers are unflattering and useful. Seventy-four percent of the college athletes evaluated experienced heat cramps. Twenty-six percent had a combination of heat syncope and heat exhaustion. The two windows of highest risk were the first three to fourteen days of practice — with the sharpest spike in the first three — and days seven and eight, when two-a-day practices started.

The conventional response to that finding is the protocol most strength-and-conditioning programs already use: ease into the volume, push fluids, watch for symptoms, pull at-risk athletes. All reasonable. None of it answers the question the study quietly raises.

The more useful question is: who exactly are the 74 percent? Pre-season practice is one of the most highly screened environments in human physical activity. These athletes are conditioned. They have access to medical staff. They drink the same water. They face the same heat. And three-quarters of them cramp anyway. The variable that explains the spread is not “fitness” in the way the locker room uses the word. It’s something the locker room doesn’t measure.

What heat actually demands of the body

Heat tolerance is a whole-system test. Maintaining a core temperature under thermal load requires the cardiovascular system to dilate peripheral blood vessels and shunt heat to the skin, the sweat-regulation system to evaporate that heat efficiently, the kidneys to manage electrolyte balance as fluid leaves, the gut to keep absorbing what’s coming in, and — load-bearing — the autonomic nervous system to coordinate all of the above in real time. When the autonomic side of that coordination is sluggish, every other downstream system runs late. Blood pressure swings. Cramping starts. The athlete who looks fine at 9 a.m. is on the ground at 11.

The conventional reading is that the athlete who cramps first is the one who trained least. In practice, the athlete who cramps first is often the one whose nervous system was already running too hot before practice started. Heat is the load that exposes them; it isn’t what made them vulnerable.

Vagal tone, sympathetic dominance, and the athlete’s invisible variable

I’ve written before about vagal tone and autonomic balance — the strength of the parasympathetic brake, indexed most often as heart rate variability. An athlete whose system already lives in sympathetic dominance — too much accelerator, too little brake — enters pre-season with a thinner thermal reserve than their training data suggests. They can run the miles. They can hit the lifts. What they cannot do, well, is regulate.

You will not see this on a depth-jump score or a 40-yard time. You will see it in heart rate variability if you measure it. You will see it in resting heart rate trends across weeks. You will see it, in clinic, in the patient who tells you they’ve always been “the one who cramps.” That sentence is more diagnostic than most coaches realize. A pattern reported across years is the body offering you data the locker room never collected.

Hidden dysfunction and the thermal layer

The Hidden Dysfunction chain — stressor → dysfunction → compensation → symptom → diagnosis — works the same way under heat as under any other load. The stressor is thermal demand. The acute dysfunction is whatever the day’s symptom looks like: cramp, dizziness, the wall-hit at the end of the second practice. The compensation is everything the athlete’s autonomic system did to keep them functional through the off-season despite already running too hot. The symptom is what shows up when the compensation runs out of headroom on day three.

Most athletes are diagnosed in the symptom layer. They are told they’re dehydrated, undertrained, or out of shape. Sometimes one of those is true. Often, none is — and what is true is a sustained sympathetic over-activation that was successfully invisible until a 95-degree afternoon made it impossible to hide. The fix isn’t more water. The fix is restoring the parasympathetic brake the athlete has been doing without for years.

What this looks like in practice

In clinic, the work has three layers. First, structural: clear cervical, cranial, and thoracic restrictions that biomechanically up-regulate the sympathetic side. The upper neck and the upper rib cage are wired to the autonomic system in ways most musculoskeletal training treats casually. Second, autonomic: dietary, breath, sleep, and direct vagal work to rebuild parasympathetic capacity. Third, monitoring: the athlete starts watching HRV trends the way they already watch sprint times. The metric is honest. The trend is teachable.

The same approach works for the patient who is not an athlete but tells me, every July, that they “can’t handle the heat anymore.” It is the same physiology. It just shows up at a lower threshold of demand because the demand is “walking from the car to the office” instead of “two-a-day practice in August.”

Who this is for

This piece is for the parent of a pre-season athlete who has been on the ground three years in a row and been told it’s hydration. For the masters runner who has watched their heat tolerance drop a decade earlier than their pace did. For the adult patient who quietly does not trust their body in summer the way they used to and assumes that’s age. It is not always age. Often it is a system that has been carrying a sympathetic load for years and lost the brake quietly enough that the loss never got named.

The locker room measures what’s easy to measure. The body measures everything. If your heat tolerance has changed and you don’t know why, the answer is usually a layer underneath the one that’s been examined.

Call the office for an intake. We’ll find out together what your autonomic system has been carrying that the symptom didn’t name.

— Dr. Robert L. Janda, MA, DC