Excerpts taken from an article written by Johnathan Sullivan, MD. in the 2013 Starting Strength blog
“Athletes who engage in serious, programmatic, heavy resistance training will do so under Valsalva – whether they want to or not, as we shall see. And a very small number of them do, in fact, suffer hemorrhagic strokes. But is this a cause-effect relationship? Is there either a physiologic or evidentiary basis for claiming that the Valsalva is unsafe under a load? Are you going to die?
The answer to the last question is definitely yes…although probably not today. The answers to the other questions are rather murkier. Let’s try for some clarity, or at least some full-frontal nerdity.
The Valsalva Maneuver: Background
Valsalva refers to a Dead Italian Dude named Antonio Maria Valsalva (1666-1723). He was a brilliant physician, surgeon and anatomist. He championed humanitarian reforms in the treatment of the mentally ill, he helped pioneer anatomic pathology, and he wore one badass wig. His work is remembered in a half-dozen eponyms: the Valsalva antrum of the ear, the aortic sinus of Valsalva, Valsalva’s muscle, Valsalva’s ligament, tineae Valsalva, and, of course, the Valsalva maneuver. He is also honored eponymously in the Valsalva device, a unit incorporated into space suits so astronauts working outside the spacecraft can pop their ears without taking off their helmets (which would defeat the purpose).
This great physician-scientist reportedly died of a stroke in Bologna at the age of 57. It is not clear whether Valsalva stroked under Valsalva, although it seems a good bet that he was not in a squat rack or a spacesuit at the time.]
The Valsalva causes a steep increase in thoracic and abdominal cavitary pressures in support of the spine is not an issue of contention [10]. This of course is the principle reason for its use in structural barbell lifts. Holding a large breath against a closed glottis creates a “balloon” of relatively incompressible gas in the thorax, and, via the diaphragm, a corresponding pressure increase in the abdomen. These pressures support the spine and resist vertebral shear forces [11,12,13] in a way that probably protects against orthopedic injury. Although no randomized trial of this hypothesis exists as far as I know, this putative, protective and desirable effect of Valsalva does not seem to be at issue.
In Phase I, we take a deep breath and hold it against a closed glottis. This produces an immediate increase in thoracic pressure and a slight increase in left ventricular stroke volume, cardiac output and blood pressure. Because cardiac output is relatively stable or slightly increased, there is little initial change in heart rate.
In Phase II, the “strain” continues. Decreased filling of the heart leads to a fall in stroke volume and cardiac output. The resultant drop in blood pressure triggers compensatory increases in heart rate and systemic vascular resistance, causing the blood pressure to rise again.
When the pressure is released in Phase III, the aorta and great vessels suddenly expand, and cardiac transmural pressures fall. This results in a further decrease in cardiac output and blood pressure. This phase is brief, as within a few heartbeats blood has filled the heart and preload has recovered.
During Phase IV, or recovery, we observe a sudden rapid rise in blood pressure, as the restored preload primes the heart for a surge in stroke volume. Increased cardiac output and vascular resistance jack up the blood pressure – the frequently-described “overshoot.” These hemodynamic responses are represented in Figure 3.
Such is the classical description of a Valsalva maneuver lasting about 20-30 seconds. The situation with exercise is more complicated, and more poorly described. Valsalva under a load tends to be rather more brief, and the hemodynamic demands of the movement are superimposed on a truncated version of the maneuver [4]. When a lifter is performing any but the most protracted squat, there may be no Phase II, because the rep just doesn’t last that long.